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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, Vol. 26, No. 9, 01.05.2006, p. 3595-609.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

van der Weyden, L, Arends, MJ, Chausiaux, OE, Ellis, PJ, Lange, UC, Surani, MA, Affara, N, Murakami, Y, Adams, DJ & Bradley, A 2006, 'Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis', MOL CELL BIOL, vol. 26, no. 9, pp. 3595-609. https://doi.org/10.1128/MCB.26.9.3595-3609.2006

APA

van der Weyden, L., Arends, M. J., Chausiaux, O. E., Ellis, P. J., Lange, U. C., Surani, M. A., Affara, N., Murakami, Y., Adams, D. J., & Bradley, A. (2006). Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis. MOL CELL BIOL, 26(9), 3595-609. https://doi.org/10.1128/MCB.26.9.3595-3609.2006

Vancouver

van der Weyden L, Arends MJ, Chausiaux OE, Ellis PJ, Lange UC, Surani MA et al. Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis. MOL CELL BIOL. 2006 May 1;26(9):3595-609. https://doi.org/10.1128/MCB.26.9.3595-3609.2006

Bibtex

@article{2252639d9d374782aca86fc1f30fc178,
title = "Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis",
abstract = "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.",
keywords = "Animals, Apoptosis, Cell Adhesion, Cell Adhesion Molecules, Cell Differentiation, Cytoskeleton, Embryo, Mammalian, Epididymis, Gene Expression, Immunoglobulins, Infertility, Male, Male, Membrane Proteins, Mice, Mice, Mutant Strains, Mutation, Oligonucleotide Array Sequence Analysis, Sperm Motility, Spermatids, Spermatogenesis, Spermatozoa, Stem Cells, Testis, Tumor Suppressor Proteins, Up-Regulation",
author = "{van der Weyden}, Louise and Arends, {Mark J} and Chausiaux, {Oriane E} and Ellis, {Peter J} and Lange, {Ulrike C} and Surani, {M Azim} and Nabeel Affara and Yoshinori Murakami and Adams, {David J} and Allan Bradley",
year = "2006",
month = may,
day = "1",
doi = "10.1128/MCB.26.9.3595-3609.2006",
language = "English",
volume = "26",
pages = "3595--609",
journal = "MOL CELL BIOL",
issn = "0270-7306",
publisher = "American Society for Microbiology",
number = "9",

}

RIS

TY - JOUR

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 -