Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis
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Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis. / van der Weyden, Louise; Arends, Mark J; Chausiaux, Oriane E; Ellis, Peter J; Lange, Ulrike C; Surani, M Azim; Affara, Nabeel; Murakami, Yoshinori; Adams, David J; Bradley, Allan.
in: MOL CELL BIOL, Jahrgang 26, Nr. 9, 01.05.2006, S. 3595-609.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis
AU - van der Weyden, Louise
AU - Arends, Mark J
AU - Chausiaux, Oriane E
AU - Ellis, Peter J
AU - Lange, Ulrike C
AU - Surani, M Azim
AU - Affara, Nabeel
AU - Murakami, Yoshinori
AU - Adams, David J
AU - Bradley, Allan
PY - 2006/5/1
Y1 - 2006/5/1
N2 - Tumor suppressor of lung cancer 1 (TSLC1), also known as SgIGSF, IGSF4, and SynCAM, is strongly expressed in spermatogenic cells undergoing the early and late phases of spermatogenesis (spermatogonia to zygotene spermatocytes and elongating spermatids to spermiation). Using embryonic stem cell technology to generate a null mutation of Tslc1 in mice, we found that Tslc1 null male mice were infertile. Tslc1 null adult testes showed that spermatogenesis had arrested at the spermatid stage, with degenerating and apoptotic spermatids sloughing off into the lumen. In adult mice, Tslc1 null round spermatids showed evidence of normal differentiation (an acrosomal cap and F-actin polarization indistinguishable from that of wild-type spermatids); however, the surviving spermatozoa were immature, malformed, found at very low levels in the epididymis, and rarely motile. Analysis of the first wave of spermatogenesis in Tslc1 null mice showed a delay in maturation by day 22 and degeneration of round spermatids by day 28. Expression profiling of the testes revealed that Tslc1 null mice showed increases in the expression levels of genes involved in apoptosis, adhesion, and the cytoskeleton. Taken together, these data show that Tslc1 is essential for normal spermatogenesis in mice.
AB - Tumor suppressor of lung cancer 1 (TSLC1), also known as SgIGSF, IGSF4, and SynCAM, is strongly expressed in spermatogenic cells undergoing the early and late phases of spermatogenesis (spermatogonia to zygotene spermatocytes and elongating spermatids to spermiation). Using embryonic stem cell technology to generate a null mutation of Tslc1 in mice, we found that Tslc1 null male mice were infertile. Tslc1 null adult testes showed that spermatogenesis had arrested at the spermatid stage, with degenerating and apoptotic spermatids sloughing off into the lumen. In adult mice, Tslc1 null round spermatids showed evidence of normal differentiation (an acrosomal cap and F-actin polarization indistinguishable from that of wild-type spermatids); however, the surviving spermatozoa were immature, malformed, found at very low levels in the epididymis, and rarely motile. Analysis of the first wave of spermatogenesis in Tslc1 null mice showed a delay in maturation by day 22 and degeneration of round spermatids by day 28. Expression profiling of the testes revealed that Tslc1 null mice showed increases in the expression levels of genes involved in apoptosis, adhesion, and the cytoskeleton. Taken together, these data show that Tslc1 is essential for normal spermatogenesis in mice.
KW - Animals
KW - Apoptosis
KW - Cell Adhesion
KW - Cell Adhesion Molecules
KW - Cell Differentiation
KW - Cytoskeleton
KW - Embryo, Mammalian
KW - Epididymis
KW - Gene Expression
KW - Immunoglobulins
KW - Infertility, Male
KW - Male
KW - Membrane Proteins
KW - Mice
KW - Mice, Mutant Strains
KW - Mutation
KW - Oligonucleotide Array Sequence Analysis
KW - Sperm Motility
KW - Spermatids
KW - Spermatogenesis
KW - Spermatozoa
KW - Stem Cells
KW - Testis
KW - Tumor Suppressor Proteins
KW - Up-Regulation
U2 - 10.1128/MCB.26.9.3595-3609.2006
DO - 10.1128/MCB.26.9.3595-3609.2006
M3 - SCORING: Journal article
C2 - 16611999
VL - 26
SP - 3595
EP - 3609
JO - MOL CELL BIOL
JF - MOL CELL BIOL
SN - 0270-7306
IS - 9
ER -