Source 1primary paper2021
Toolkit/Opto-Rho1DN
Opto-Rho1DN
Also known as: CIBN-pmGFP, CRY2-Rho1DN
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Opto-Rho1DN is a multi-component optogenetic switch that inhibits Rho1 by light-dependent recruitment of a dominant-negative Rho1 construct to the plasma membrane. The listed components are CIBN-pmGFP and CRY2-Rho1DN.
Usefulness & Problems
Why this is useful
This system enables acute optical inhibition of Rho1-linked actomyosin function during Drosophila mesoderm invagination. It is useful for perturbing protein localization with light rather than relying on constitutive genetic inhibition.
Source:
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Source:
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Source:
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Problem solved
It addresses the need for temporally controlled inhibition of Rho1 during morphogenesis. The cited study used optogenetic acute inhibition of actomyosin to test stage-specific mechanical requirements during mesoderm invagination.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
dominant-negative inhibitionlight-dependent plasma membrane recruitmentmembrane recruitmentMembrane RecruitmentTechniques
No technique tags yet.
Target processes
localizationInput: Light
Implementation Constraints
The system is described as comprising CIBN-pmGFP and CRY2-Rho1DN, indicating a two-component construct design based on membrane-anchored CIBN and a CRY2-fused dominant-negative Rho1 cargo. The evidence supports plasma membrane recruitment under light, but it does not provide illumination parameters, expression strategy, or cofactor requirements.
The supplied evidence does not report quantitative performance metrics such as recruitment kinetics, dynamic range, reversibility, or wavelength dependence. Independent replication, use outside the reported Drosophila context, and direct biochemical characterization are not documented in the provided material.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2primary paper2021
Source 3primary paper2021
Ranked Claims
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Approval Evidence
3 sources15 linked approval claimsfirst-pass slug opto-rho1dn
we generated an optogenetic tool, ‘Opto-Rho1DN,’ to inhibit Rho1 through light-dependent plasma membrane recruitment of a dominant negative form of Rho1 (Rho1DN).
Source:
we generated an optogenetic tool, 'Opto-Rho1DN,' to inhibit Rho1 through light-dependent plasma membrane recruitment of a dominant negative form of Rho1 (Rho1DN).
Source:
we generated an optogenetic tool, ‘Opto-Rho1DN,’ to inhibit Rho1 through light-dependent plasma membrane recruitment of a dominant negative form of Rho1 (Rho1DN)
Source:
comparative observationsupports
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Source:
comparative observationsupports
The lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination, based on comparison between wild-type and snail mutants.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
Source:
mechanismsupports
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the folding step after a stereotyped transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, 'priming' stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Source:
mechanismsupports
Optogenetic-mediated acute inhibition of actomyosin during Drosophila mesoderm invagination shows that actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a transitional configuration.
By optogenetic-mediated acute inhibition of actomyosin, we find that during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration.
Source:
mechanistic inferencesupports
The binary response to acute actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
Source:
mechanistic modelsupports
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
Source:
modeling resultsupports
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Source:
model recapitulationsupports
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression from apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Source:
model recapitulationsupports
Computer modeling recapitulated the binary tissue response to actomyosin inhibition using a simulated epithelium with mesoderm apical constriction and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Computer modeling analysis demonstrates that the binary tissue response to actomyosin inhibition can be recapitulated in the simulated epithelium that undergoes buckling-like deformation jointly mediated by apical constriction in the mesoderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
Source:
observationsupports
Comparison between wild-type and snail mutants indicates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Source:
stage dependent requirementsupports
During Drosophila mesoderm invagination, actomyosin contractility is required to prevent tissue relaxation during the early priming stage but is dispensable for the later folding step after a stereotyped transitional configuration.
during Drosophila mesoderm invagination, actomyosin contractility is critical to prevent tissue relaxation during the early, ‘priming’ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration
Source:
state propertysupports
The binary response to actomyosin inhibition suggests that the Drosophila mesoderm is mechanically bistable during gastrulation.
This binary response suggests that Drosophila mesoderm is mechanically bistable during gastrulation.
Source:
tool functionsupports
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Source:
tool functionsupports
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Taken together, our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
Source:
tool functionsupports
Opto-Rho1DN is an effective tool for spatially and temporally confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly.
our results indicate that Opto-Rho1DN is an effective tool for spatially- and temporally-confined inactivation of apical actomyosin contractility through simultaneous myosin inactivation and actin disassembly
Source:
Comparisons
Source-backed strengths
The evidence states that Opto-Rho1DN was generated specifically for light-dependent plasma membrane recruitment of dominant-negative Rho1, providing an acute optogenetic inhibition strategy. In the associated study context, optogenetic acute inhibition revealed that actomyosin contractility is required during an early priming stage but becomes dispensable after a transitional configuration in later folding.
Source:
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination.
Source:
comparison between wild-type and snail mutants that fail to specify the mesoderm demonstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently of mesoderm invagination
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