TY - JOUR
T1 - EFF-1 is sufficient to initiate and execute tissue-specific cell fusion in C. elegans
AU - Shemer, Gidi
AU - Suissa, Meital
AU - Kolotuev, Irina
AU - Nguyen, Ken C.Q.
AU - Hall, David H.
AU - Podbilewicz, Benjamin
N1 - Funding Information:
We thank A. Newman for AC unpublished results. J. Novelli, J. Hodgkin, and N. Pujol for the isolation and initial characterization of eff-1(np29). A. Fire for pPD49.78 and J. Simske for ajm-1::gfp. C. Marks, G. Stephney, M. Rosenberg, S. Weisman, and Y. Talmon for help with electron microscopy. A. Mittal, C. Ramos, G. Leikina, H. Delanoe, E. Zaitseva, M. Glickman, J. Zimmerberg, Y, Rabin, S. Hess, P. Blank, and G. Gattegno for discussions. M. Krause, S. Vogel, M. Kozlov, Y. Gruenbaum, K. Melikov, and L. Chernomordik for critically reading this manuscript. This research was supported by grants from National Institutes of Health (grant number RR 12596), and the Center for C. elegans Anatomy to D.H.H., Israel Science Foundation - The Charles H. Revson Foundation, Binational Science Foundation, Fund for the Promotion of Research at the Technion, and Human Frontiers Science Program (HFSP) to B.P.
PY - 2004/9/7
Y1 - 2004/9/7
N2 - Despite the identification of essential processes in which cell fusion plays spectacular roles such as in fertilization and development of muscle, bone, and placenta [1-5], there are no identified proteins that directly mediate developmental cell fusion reactions. C. elegans has recently become among the best-characterized models to use for studying developmental cell fusion [5-15]. The eff-1 (epithelial fusion failure) gene encodes novel type I membrane proteins required for epithelial cell fusion. Analysis of eff-1 mutants showed that cell fusion normally restricts routes for cell migration and establishes body and organ shape and size [ 5, 8, 9, 11]. Here, we explored cell fusion by using time-lapse confocal and electron microscopy of different organs. We found that ectopic expression of eff-1 is sufficient to fuse epithelial cells that do not normally fuse. This ectopic fusion results in cytoplasmic content mixing and disappearance of apical junctions, starting less than 50 min after the start of eff-1 transcription. We found that eff-1 is necessary to initiate and expand multiple microfusion events between pharyngeal muscle cells. Surprisingly, eff-1 is not required to fuse the gonadal anchor cell to uterine cells. Thus, eff-1 is sufficient and essential for most but not all cell fusion events during C. elegans development.
AB - Despite the identification of essential processes in which cell fusion plays spectacular roles such as in fertilization and development of muscle, bone, and placenta [1-5], there are no identified proteins that directly mediate developmental cell fusion reactions. C. elegans has recently become among the best-characterized models to use for studying developmental cell fusion [5-15]. The eff-1 (epithelial fusion failure) gene encodes novel type I membrane proteins required for epithelial cell fusion. Analysis of eff-1 mutants showed that cell fusion normally restricts routes for cell migration and establishes body and organ shape and size [ 5, 8, 9, 11]. Here, we explored cell fusion by using time-lapse confocal and electron microscopy of different organs. We found that ectopic expression of eff-1 is sufficient to fuse epithelial cells that do not normally fuse. This ectopic fusion results in cytoplasmic content mixing and disappearance of apical junctions, starting less than 50 min after the start of eff-1 transcription. We found that eff-1 is necessary to initiate and expand multiple microfusion events between pharyngeal muscle cells. Surprisingly, eff-1 is not required to fuse the gonadal anchor cell to uterine cells. Thus, eff-1 is sufficient and essential for most but not all cell fusion events during C. elegans development.
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U2 - 10.1016/j.cub.2004.07.059
DO - 10.1016/j.cub.2004.07.059
M3 - Article
C2 - 15341747
AN - SCOPUS:4644367201
SN - 0960-9822
VL - 14
SP - 1587
EP - 1591
JO - Current Biology
JF - Current Biology
IS - 17
ER -