AFF-1, a FOS-1-Regulated Fusogen, Mediates Fusion of the Anchor Cell in C. elegans

Amir Sapir; Jaebok Choi; Evgenia Leikina; Ori Avinoam; Clari Valansi; Leonid V. Chernomordik; Anna P. Newman; Benjamin Podbilewicz

doi:10.1016/j.devcel.2007.03.003

AFF-1, a FOS-1-Regulated Fusogen, Mediates Fusion of the Anchor Cell in C. elegans

Amir Sapir, Jaebok Choi, Evgenia Leikina, Ori Avinoam, Clari Valansi, Leonid V. Chernomordik, Anna P. Newman, Benjamin Podbilewicz

Research output: Contribution to journal › Article › peer-review

Abstract

Cell fusion is fundamental for reproduction and organ formation. Fusion between most C. elegans epithelial cells is mediated by the EFF-1 fusogen. However, fusion between the anchor cell and the utse syncytium that establishes a continuous uterine-vulval tube proceeds normally in eff-1 mutants. By isolating mutants where the anchor-cell fails to fuse, we identified aff-1. AFF-1 ectopic expression results in fusion of cells that normally do not fuse in C. elegans. The fusogen activity of AFF-1 was further confirmed by its ability to fuse heterologous cells. AFF-1 and EFF-1 differ in their fusogenic activity and expression patterns but share eight conserved predicted disulfide bonds in their ectodomains, including a putative TGF-β-type-I-Receptor domain. We found that FOS-1, the Fos transcription factor ortholog that controls anchor-cell invasion during nematode development, is a specific activator of aff-1-mediated anchor-cell fusion. Thus, FOS-1 links cell invasion and fusion in a developmental cascade.

Original language	English
Pages (from-to)	683-698
Number of pages	16
Journal	Developmental Cell
Volume	12
Issue number	5
DOIs	https://doi.org/10.1016/j.devcel.2007.03.003
State	Published - 8 May 2007
Externally published	Yes

Bibliographical note

Funding Information:
We thank Y. Kohara for EST clones, A. Fire for vectors, S. Mitani and the NBRP for the aff-1(tm2214) deletion allele, T. Stiernagle and the Caenorhabditis Genetics Center for nematode strains, F. Rey for advice on structural domain interpretation, M. Akerman for bioinformatics advice, and M. Suissa, S. Joshua, K. Brunschwig, D. Cassel, Y. Gruenbaum, E. Schejter, and B-Z Shilo for critically reading the manuscript. This research was supported by grants from the Israel Science Foundation (B.P.) and by the Intramural Research Program of the National Institute of Child Health and Human Development, National Institutes of Health (L.V.C.).

Keywords

CELLBIO
DEVBIO

ASJC Scopus subject areas

Molecular Biology
General Biochemistry, Genetics and Molecular Biology
Developmental Biology
Cell Biology

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10.1016/j.devcel.2007.03.003

Cite this

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title = "AFF-1, a FOS-1-Regulated Fusogen, Mediates Fusion of the Anchor Cell in C. elegans",

abstract = "Cell fusion is fundamental for reproduction and organ formation. Fusion between most C. elegans epithelial cells is mediated by the EFF-1 fusogen. However, fusion between the anchor cell and the utse syncytium that establishes a continuous uterine-vulval tube proceeds normally in eff-1 mutants. By isolating mutants where the anchor-cell fails to fuse, we identified aff-1. AFF-1 ectopic expression results in fusion of cells that normally do not fuse in C. elegans. The fusogen activity of AFF-1 was further confirmed by its ability to fuse heterologous cells. AFF-1 and EFF-1 differ in their fusogenic activity and expression patterns but share eight conserved predicted disulfide bonds in their ectodomains, including a putative TGF-β-type-I-Receptor domain. We found that FOS-1, the Fos transcription factor ortholog that controls anchor-cell invasion during nematode development, is a specific activator of aff-1-mediated anchor-cell fusion. Thus, FOS-1 links cell invasion and fusion in a developmental cascade.",

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author = "Amir Sapir and Jaebok Choi and Evgenia Leikina and Ori Avinoam and Clari Valansi and Chernomordik, {Leonid V.} and Newman, {Anna P.} and Benjamin Podbilewicz",

note = "Funding Information: We thank Y. Kohara for EST clones, A. Fire for vectors, S. Mitani and the NBRP for the aff-1(tm2214) deletion allele, T. Stiernagle and the Caenorhabditis Genetics Center for nematode strains, F. Rey for advice on structural domain interpretation, M. Akerman for bioinformatics advice, and M. Suissa, S. Joshua, K. Brunschwig, D. Cassel, Y. Gruenbaum, E. Schejter, and B-Z Shilo for critically reading the manuscript. This research was supported by grants from the Israel Science Foundation (B.P.) and by the Intramural Research Program of the National Institute of Child Health and Human Development, National Institutes of Health (L.V.C.). ",

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AU - Sapir, Amir

AU - Choi, Jaebok

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AU - Avinoam, Ori

AU - Valansi, Clari

AU - Chernomordik, Leonid V.

AU - Newman, Anna P.

AU - Podbilewicz, Benjamin

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N2 - Cell fusion is fundamental for reproduction and organ formation. Fusion between most C. elegans epithelial cells is mediated by the EFF-1 fusogen. However, fusion between the anchor cell and the utse syncytium that establishes a continuous uterine-vulval tube proceeds normally in eff-1 mutants. By isolating mutants where the anchor-cell fails to fuse, we identified aff-1. AFF-1 ectopic expression results in fusion of cells that normally do not fuse in C. elegans. The fusogen activity of AFF-1 was further confirmed by its ability to fuse heterologous cells. AFF-1 and EFF-1 differ in their fusogenic activity and expression patterns but share eight conserved predicted disulfide bonds in their ectodomains, including a putative TGF-β-type-I-Receptor domain. We found that FOS-1, the Fos transcription factor ortholog that controls anchor-cell invasion during nematode development, is a specific activator of aff-1-mediated anchor-cell fusion. Thus, FOS-1 links cell invasion and fusion in a developmental cascade.

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ER -

AFF-1, a FOS-1-Regulated Fusogen, Mediates Fusion of the Anchor Cell in C. elegans

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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