# hbl-1 does not contribute to the misexpression of an adult cell fate marker in daf-16 mutant dauer larvae

## TL;DR

This study shows that the gene hbl-1 does not help control a specific cell marker in worm larvae lacking daf-16.

## Contribution

The paper clarifies that hbl-1 is not a downstream regulator of daf-16 in dauer larvae.

## Key findings

- A gain-of-function hbl-1 allele does not suppress col-19p::gfp expression in daf-16 mutant dauer larvae.
- HBL-1 protein is not detectable in control or daf-16 mutant dauer larvae.
- HBL-1 does not function downstream of DAF-16 to regulate col-19p::gfp expression.

## Abstract

In

Caenorhabditis elegans

dauer larvae, the FOXO ortholog,

daf-16

, opposes the expression of the
col-19p::gfp
adult cell fate marker in the lateral hypodermis.

daf-16

acts in part via

lin-41
,

a heterochronic gene that promotes larval seam cell fate during non-dauer development. Here, we show that a different heterochronic gene,

hbl-1

, does not function downstream of

daf-16

to regulate
col-19p::gfp
expression during dauer. A gain-of-function

hbl-1

allele did not suppress ectopic
col-19p::gfp
expression in

daf-16
(0)

dauer larvae, and
HBL-1
protein was not detectable in control or

daf-16
(0)

dauer larvae.