Role of C. elegans lin-40 MTA in vulval fate specification and morphogenesis-Reference-Cited by-同舟云学术

Role of C. elegans lin-40 MTA in vulval fate specification and morphogenesis

Published:2001-12-01 Issue:23 Volume:128 Page:4911-4921
ISSN:1477-9129
Container-title:Development
language:en
Short-container-title:

Author:

Chen Zhe,Han Min¹

Affiliation:

1. Howard Hughes Medical Institute, Department of Molecular, Cellular and Developmental Biology, University of Colorado at Boulder, Boulder, CO 80309, USA

Abstract

Vulval differentiation in Caenorhabditis elegans involves several fundamental cellular events, including cell fusion, division and migration. We have characterized the role of the lin-40 (also known as egr-1) gene in these cellular processes. LIN-40 is homologous to the metastasis-associated factor 1 (MTA1) in mammals, which has been identified as a component of the nucleosome remodeling and histone deacetylation (NuRD) complex that functions as a transcriptional co-repressor. We show here that lin-40 negatively regulates vulval fate specification at least partly by promoting cell fusion between the vulval precursor cells and the hypodermal syncytium at an early larval stage. This inhibitory function of lin-40 might be carried out by downregulating lin-39 Hox expression. We also show that lin-40 is specifically required for cell divisions along the transverse orientation during vulval morphogenesis.

Publisher

The Company of Biologists

Subject

Developmental Biology,Molecular Biology

Link

http://journals.biologists.com/dev/article-pdf/128/23/4911/1138425/4911.pdf

Reference53 articles.

1. Ahringer, J. (2000). NuRD and SIN3 histone deacetylase complexes in development. Trends Genet.16, 351-356.

2. Beitel, G. J., Clark, S. G. and Horvitz, H. R. (1990). Caenorhabditis elegans ras gene let-60 acts as a switch in the pathway of vulval induction. Nature348, 503-509.

3. Bettinger, J. C., Lee, K. and Rougvie, A. E. (1996). Stage-specific accumulation of the terminal differentiation factor LIN- 29 during Caenorhabditis elegans development. Development122, 2517-2527.

4. Brehm, A., Miska, E. A., McCance, D. J., Reid, J. L., Bannister, A. J. and Kouzarides, T. (1998). Retinoblastoma protein recruits histone deacetylase to repress transcription. Nature391, 597-601.

5. Brenner, S. (1974). The genetics of Caenorhabditis elegans. Genetics77, 71-94.

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