Catharine H. Rankin

This study identifies a new role for NHR-49 in promoting attractive chemotaxis in C. elegans, independent of its known role in fatty acid metabolism.

The paper analyzes reversal speed plasticity in C. elegans during mechanosensory habituation and identifies neuropeptide signaling as involved in early speed modulation.

The paper evaluates phenotypic variation among unc-43 LOF alleles in C. elegans to identify reliable reference alleles for future studies.

This study shows ethanol modulates habituation in C. elegans via the BK channel SLO-1 through a novel mechanism, altering response plasticity without general facilitation or inhibition.

This study shows that a familial Alzheimer's disease mutation in presenilin-1 causes cell-specific neurodegeneration in C. elegans independent of amyloid-beta, which is rescued by over-expression of wild-type human presenilin.

The paper assesses the temporal function and phenotypic reversibility of neurodevelopmental disorder risk genes in C. elegans using a conditional degradation system and machine vision, finding varying degrees of reversibility across genes and phenotypes.

The paper adapts peel-1 negative selection to CRISPR-Cas9 genome editing in C. elegans, enabling automated screening-free generation and phenotyping of genome-edited animals.

The paper evaluates 106 PTEN variants using 18 assays across 5 models to identify molecular mechanisms of dysfunction, finding that stability and domain-specific assays are critical for accurate impact assessment.

This study systematically analyzes ASD-associated genes in C. elegans, identifying phenotypic relationships and reversible impairments in habituation learning.

This study shows that CMK-1 and OGT-1 modulate mechanosensory responses and habituation in C. elegans, with effects dependent on interstimulus interval.

This paper uses CRISPR-Cas9 in C. elegans to replace human genes and assess their function, showing it can classify disease variants accurately.