# Increased expression of metabolism and lysosome-associated genes in a C. elegans dpy-7 cuticle furrow mutant

## TL;DR

This study shows that a C. elegans cuticle mutant increases specific genes related to metabolism and lysosomes, possibly through mechanisms separate from SKN-1.

## Contribution

The study confirms RNAseq findings using RT-qPCR and reveals that gene activation in cuticle mutants is not dependent on SKN-1.

## Key findings

- Five genes related to redox balance, ATP homeostasis, and lysosome function are upregulated in dpy-7 mutants.
- SKN-1 RNAi does not reduce the expression of these genes, indicating alternative regulatory pathways.
- The study highlights a potential new regulatory mechanism for gene expression in response to cuticle damage.

## Abstract

The collagen-based epidermal ‘cuticle' of
Caenorhabditis elegans
functions as an extracellular sensor for damage that regulates genes promoting osmotic balance, innate immunity, and detoxification. Prior studies demonstrate that
SKN-1
, an ortholog of the mammalian Nrf transcription factors, activates core detoxification genes downstream from cuticle damage. Prior RNAseq data suggested that expression of five genes with functions in redox balance, ATP homeostasis, and lysosome function (

gst-15

,

gst-24

,

cyts-1

,

argk-1

, and

mfsd-8.4

) were increased in a cuticle collagen mutant; this study employed RT-qPCR to verify this observation and to test the role of
SKN-1
. Activation of all five genes was verified in

dpy-7

mutants, but none were reduced by

skn-1
(RNAi)

suggesting parallel or distinct regulatory mechanisms.