Toolkit/SCFTIR1 E3 ubiquitin ligase complex

SCFTIR1 E3 ubiquitin ligase complex

Construct Pattern·Research·Since 2005

Also known as: SCFTIR1

Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.

Summary

Auxin signalling is mediated, at least in large part, by an SCFTIR1 E3 ubiquitin ligase complex that accelerates Aux/IAA repressor degradation in response to IAA, thereby altering gene expression.

Usefulness & Problems

Why this is useful

This complex is described as a major mediator of auxin signaling that accelerates degradation of Aux/IAA repressors in response to IAA. The resulting change in repressor abundance alters gene expression.; auxin-responsive protein degradation; auxin signaling studies; linking small-molecule auxin input to transcriptional output

Source:

This complex is described as a major mediator of auxin signaling that accelerates degradation of Aux/IAA repressors in response to IAA. The resulting change in repressor abundance alters gene expression.

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auxin-responsive protein degradation

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auxin signaling studies

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linking small-molecule auxin input to transcriptional output

Problem solved

It provides a mechanistic link between auxin presence and downstream transcriptional response through targeted proteolysis.; mediates auxin-dependent degradation of Aux/IAA repressors; provides a mechanism for converting IAA perception into altered gene expression

Source:

It provides a mechanistic link between auxin presence and downstream transcriptional response through targeted proteolysis.

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mediates auxin-dependent degradation of Aux/IAA repressors

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provides a mechanism for converting IAA perception into altered gene expression

Problem links

mediates auxin-dependent degradation of Aux/IAA repressors

Literature

It provides a mechanistic link between auxin presence and downstream transcriptional response through targeted proteolysis.

Source:

It provides a mechanistic link between auxin presence and downstream transcriptional response through targeted proteolysis.

provides a mechanism for converting IAA perception into altered gene expression

Literature

It provides a mechanistic link between auxin presence and downstream transcriptional response through targeted proteolysis.

Source:

It provides a mechanistic link between auxin presence and downstream transcriptional response through targeted proteolysis.

Taxonomy & Function

Primary hierarchy

Mechanism Branch

Architecture: A reusable architecture pattern for arranging parts into an engineered system.

Techniques

No technique tags yet.

Target processes

degradationsignaling

Implementation Constraints

cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: regulator

Its action is described in the context of IAA and Aux/IAA repressors, so those signaling components are prerequisites in the reviewed mechanism.; requires auxin/IAA-responsive context; depends on Aux/IAA repressor substrates

The abstract does not claim that SCFTIR1 alone explains all auxin signaling or broader auxin metabolism and transport.; the review states signaling is mediated at least in large part by this complex, implying the mechanism is not fully exhaustive

Validation

Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication

Supporting Sources

Ranked Claims

Claim 1review summarysupports2005Source 1needs review

Auxin signaling is mediated at least in large part by an SCFTIR1 E3 ubiquitin ligase complex that accelerates Aux/IAA repressor degradation in response to IAA, thereby altering gene expression.

Approval Evidence

1 source1 linked approval claimfirst-pass slug scftir1-e3-ubiquitin-ligase-complex
Auxin signalling is mediated, at least in large part, by an SCFTIR1 E3 ubiquitin ligase complex that accelerates Aux/IAA repressor degradation in response to IAA, thereby altering gene expression.

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review summarysupports

Auxin signaling is mediated at least in large part by an SCFTIR1 E3 ubiquitin ligase complex that accelerates Aux/IAA repressor degradation in response to IAA, thereby altering gene expression.

Source:

Comparisons

Source-stated alternatives

The review also discusses auxin transport, biosynthesis, conjugation, and hormone interactions as other layers controlling auxin response.

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The review also discusses auxin transport, biosynthesis, conjugation, and hormone interactions as other layers controlling auxin response.

Source-backed strengths

presented as a major mediator of auxin signaling; connects hormone response to regulated proteolysis

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presented as a major mediator of auxin signaling

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connects hormone response to regulated proteolysis

Compared with CAR-NK cells

SCFTIR1 E3 ubiquitin ligase complex and CAR-NK cells address a similar problem space because they share degradation, signaling.

Shared frame: same top-level item type; shared target processes: degradation, signaling; shared mechanisms: degradation

Relative tradeoffs: appears more independently replicated; looks easier to implement in practice.

SCFTIR1 E3 ubiquitin ligase complex and Jalpha helix point mutations disrupting LOV-domain interaction address a similar problem space because they share degradation, signaling.

Shared frame: same top-level item type; shared target processes: degradation, signaling; shared mechanisms: degradation

Strengths here: looks easier to implement in practice.

SCFTIR1 E3 ubiquitin ligase complex and PCB synthesis expression vector address a similar problem space because they share degradation, signaling.

Shared frame: same top-level item type; shared target processes: degradation, signaling; shared mechanisms: degradation

Strengths here: looks easier to implement in practice; may avoid an exogenous cofactor requirement.

Ranked Citations

  1. 1.
    StructuralSource 1Annals of Botany2005Claim 1

    Seeded from load plan for claim claim_2. Extracted from this source document.