field-evolved resistance ... can threaten their long-term efficacy
First-pass extracted concept
field-evolved resistance to Bt Cry toxins
Evidence Snippets
Supporting Sources
Linked Claims
Future sustainability of Bt biotechnology depends on integrating single-cell transcriptomics, midgut-specific CRISPR screens, microbiome engineering, and AI-accelerated protein design to preempt resistance trajectories.
Future sustainability hinges on system-level integration of single-cell transcriptomics, midgut-specific CRISPR screens, microbiome engineering, and AI-accelerated protein design to preempt resistance trajectories
Resistance arises from target-site alterations such as ABCC2/ABCC3 and cadherin mutations, altered midgut protease profiles, enhanced immune regeneration, and microbiota-mediated detoxification.
Resistance arises from target-site alterations (e.g., ABCC2/ABCC3, Cadherin mutations), altered midgut protease profiles, enhanced immune regeneration, and microbiota-mediated detoxification
Field-evolved resistance to Bt Cry toxins in lepidopteran pests is mediated by multilayered mechanisms beyond the classical pore-formation model, including signaling, immune, and microbiota-linked processes.
Beyond the classical pore-formation model, emerging evidence highlights signal transduction cascades, immune evasion via suppression of Toll/IMD pathways, and tripartite toxin-host-microbiota interactions
The resistance framework includes transcription factor networks, constitutive MAPK hyperactivation especially MAP4K4-driven cascades, and preliminary non-coding RNA involvement.
orchestrated by transcription factor networks (GATA, FoxA, FTZ-F1), constitutive MAPK hyperactivation (especially MAP4K4-driven cascades), along with preliminary emerging findings on non-coding RNA involvement