The role of lin-12 notch in C. elegans anchor cell proliferation.

Abstract

The gonadal anchor cell (AC) is an essential organizer for the development of the egg-laying organ in the C. elegans hermaphrodite. Recent work has investigated the mechanisms that control the quiescent state the AC adopts while fulfilling its functions. In this context, the transcription factors EGL-43 and NHR-67 are required to maintain the G1 cell cycle arrest of the AC and prevent proliferation. While NHR-67 acts primarily by up-regulating the CDK inhibitor CKI-1, the role of EGL-43 in this process has been subject to debate. Deng et al. (2020) reported that inhibition of the notch receptor lin-12 by RNAi partially suppressed the AC proliferation phenotype caused by egl-43 RNAi. By contrast, Martinez et al. (2022) found that down-regulation of LIN-12 NOTCH via the auxin-inducible degradation system did not reduce AC proliferation. To resolve this issue, we performed egl-43 RNAi in the background of a lin-12 null allele and observed a similar suppression of AC proliferation as reported previously by Deng et al. (2020). Hence, AC proliferation caused by the downregulation of egl-43 partially depends on LIN-12 NOTCH signaling.