Mouse TEX14 is required for embryonic germ cell intercellular bridges but not female fertility.
A conserved feature of germ cell cytokinesis is the formation of stable intercellular bridges between daughter cells. These intercellular bridges are seen in diverse species from Drosophila melanogaster to Homo sapiens and have been shown to have roles in communication of large numbers of germ cells. In testis expressed gene 14 (Tex14) knockout mice, intercellular bridges do not form during spermatogenesis, and male mice are sterile, demonstrating an essential role for intercellular bridges in postnatal spermatogenesis in mammals. Intercellular bridges also form between dividing germ cells in both male and female embryos. However, little is known about the formation or role of the embryonic intercellular bridges in mammals. In females, embryonic intercellular bridges have been proposed to have a role in development of the presumptive oocyte. Herein, we show that TEX14 is an essential component of male and female embryonic intercellular bridges. In addition, we demonstrate that mitotic kinesin-like protein 1 (MKLP1, official symbol KIF23), which we have discovered is a component of intercellular bridges during spermatogenesis, is also a component of male and female embryonic intercellular bridges. Germ cell intercellular bridges are readily identified by KIF23 immunofluorescence between the gonocytes and oogonia of control mice but are absent between germ cells of Tex14-null mice. Furthermore, by electron microscopy, intercellular bridges are present in all control newborn ovaries but are absent in the Tex14 knockout ovaries. Despite the absence of embryonic intercellular bridges in the Tex14-null mice, male mice initiate spermatogenesis, and female mice are fertile. Although fewer oocytes were present in Tex14-null neonatal ovaries, folliculogenesis was still active at 1 yr of age. Thus, while TEX14 and intercellular bridges have an essential role in postnatal spermatogenesis, they are not required in the embryo.
Greenbaum
Michael P
MP
Department of Pathology, Baylor College of Medicine, Houston, Texas 77030, USA.
Iwamori
Naoki
N
Agno
Julio E
JE
Matzuk
Martin M
MM
D000818:Animals; D002450:Cell Communication / Q000502:physiology*; D048749:Cytokinesis / Q000502:physiology; D005260:Female; D005298:Fertility / Q000502:physiology*; D005854:Germ Cells / Q000166:cytology / Q000378:metabolism*; D016547:Kinesins / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009865:Oocytes / Q000166:cytology; D009866:Oogenesis / Q000502:physiology; D010053:Ovary / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D013091:Spermatogenesis / Q000502:physiology; D013737:Testis / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
C510086:TEX14 protein, mouse; D014157:Transcription Factors; D017346:Protein Serine-Threonine Kinases; C541430:MKLP1 protein, mouse; D016547:Kinesins