TEX14 is essential for intercellular bridges and fertility in male mice

doi:10.1073/pnas.0505123103

TEX14 is essential for intercellular bridges and fertility in male mice

Departments of *Pathology,
^†Molecular and Human Genetics,
^‖Molecular and Cellular Biology, and
^††Obstetrics and Gynecology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030;
^§Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557; and
**Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195

Edited by Ryuzo Yanagimachi, University of Hawaii, Honolulu, HI, and approved January 30, 2006
↵ ^‡M.P.G. and W.Y. contributed equally to this work. (received for review June 17, 2005)

Abstract

Cytokinesis in somatic cells concludes with the formation of a midbody, which is abscised to form individual daughter cells. In contrast, germ cell cytokinesis results in a permanent intercellular bridge connecting the daughter cells through a large cytoplasmic channel. During spermatogenesis, proposed roles for the intercellular bridge include germ cell communication, synchronization, and chromosome dosage compensation in haploid cells. Although several essential components of the midbody have recently been identified, essential components of the vertebrate germ cell intercellular bridge have until now not been described. Herein, we show that testis-expressed gene 14 (TEX14) is a novel protein that localizes to germ cell intercellular bridges. In the absence of TEX14, intercellular bridges are not observed by using electron microscopy and other markers. Spermatogenesis in Tex14 ^−/− mice progresses through the transit amplification of diploid spermatogonia and the expression of early meiotic markers but halts before the completion of the first meiotic division. Thus, TEX14 is required for intercellular bridges in vertebrate germ cells, and these studies provide evidence that the intercellular bridge is essential for spermatogenesis and fertility.

Footnotes

^‡‡To whom correspondence should be addressed. E-mail: mmatzuk{at}bcm.tmc.edu
↵ ^¶Present address: Department of Obstetrics and Gynecology and Institute of Clinical Medicine, National Cheng Kung University, College of Medicine, Tainan 70428, Taiwan.
Author contributions: M.P.G., R.E.B., and M.M.M. designed research; M.P.G., W.Y., J.E.A., M.S., and M.M.M. performed research; M.-H.W. and Y.-N.L. contributed new reagents/analytic tools; M.P.G., W.Y., R.E.B., A.R., and M.M.M. analyzed data; and M.P.G., R.E.B., and M.M.M. wrote the paper.
Conflict of interest statement: No conflicts declared.
This paper was submitted directly (Track II) to the PNAS office.
Abbreviations:

HSF2,

heat-shock factor 2;

SYCP3,

synaptonemal complex protein 3;

CCNA1,

cyclin A1;

TEX14,

testis-expressed gene 14;

PLZF,

promyelocytic leukemia zinc finger.