Schnabel R et al. (1997) Nature "Hox genes misled by local environments."

Schnabel R, Schnabel H

[Nature, 1997]

Cowing and Kenyon raise an important issue concerning Hox genes by suggesting that these genes may not only be expressed according to position but also according to cell lineage. This suggestion is based on two experiments in which the so-called M cell and two hypodermal V6 cells were manipulated to express a Hox gene, mab-5, outside the posterior region of the Caenorhabditis elegans embryo. Here we propose a less radical interpretation of these data.

Abete-Luzi P et al. (2018) Genesis "Regulation of C. elegans L4 cuticle collagen genes by the heterochronic protein LIN-29."

Abete-Luzi P, Eisenmann DM

[Genesis, 2018]

The cuticle, the outer covering of the nematode C. elegans, is synthesized five times during the worm's life by the underlying hypodermis. Cuticle collagens, the major cuticle component, are encoded by a large family of col genes and, interestingly, many of these genes express predominantly at a single developmental stage. This temporal preference motivated us to investigate the mechanisms underlying col gene expression and here we focus on a subset of col genes expressed in the L4 stage. We identified minimal promoter regions of <300 bp for col-38, col-49, and col-63. In these regions, we predicted cis-regulatory sequences and evaluated their function in vivo via mutagenesis of a col-38p::yfp reporter. We used RNAi to study the requirement for candidate transcription regulators ELT-1 and ELT-3, LIN-29, and the LIN-29 co-factor MAB-10, and found LIN-29 to be necessary for the expression of four L4-specific genes (col-38, col-49, col-63 and col-138). Temporal misexpression of LIN-29 was also sufficient to activate these genes at a different developmental stage. The LIN-29 DNA-binding domain bound the col-38, col-49, and col-63 minimal promoters in vitro. For col-38 we showed that the LIN-29 sites necessary for reporter expression in vivo are also bound in vitro: this is the first identification of specific binding sites for LIN-29 necessary for in vivo target gene expression. This article is protected by copyright. All rights reserved.