Xiaofei Bai

This study identifies molecular mechanisms governing PIEZO channel trafficking in C. elegans germline, showing dependence on RAB-11 and structural integrity, with implications for channelopathies.

The paper identifies genetic suppressors of FASN dysfunction in C. elegans by using temperature-sensitive mutants and CRISPR/Cas9 to rescue embryonic lethality.

This study identifies BLTP2 as a pro-survival protein that regulates phosphatidylethanolamine levels in the plasma membrane to maintain its fluidity and function, linking it to cancer aggressiveness.

The paper shows that the C. elegans PIEZO channel regulates pharyngeal movement by sensing food accumulation in the intestine.

This study identifies genetic suppressors of a BSCL2 pathogenic variant in C. elegans, revealing potential interactors and pathways involved in seipin function.

This study identifies gex-3 as a suppressor of a PIEZO-1 gain-of-function mutation in C. elegans, revealing a role for the cytoskeleton in regulating PIEZO channel activity.

This study identifies distinct pezo-1 isoforms in C. elegans with tissue-specific expression and functional roles in food intake regulation.

The paper shows malonyl-CoA is transported from the soma to the germline via gap junctions in C. elegans to support embryogenesis.

This study identifies PEZO-1 as critical for ovulation and fertilization in C. elegans by coordinating reproductive tissues through mechanical sensing and calcium signaling.

The paper investigates cytokinesis variations during C. elegans embryonic morphogenesis and finds Aurora B kinase is essential for epithelial polarization and tissue formation.

This study identifies novel separase regulators in C. elegans through an ENU mutagenesis screen, revealing mutations in pph-5 and hsp-90 that suppress a separase mutant phenotype.