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Mol. Cells 2013; 35(1): 54-60

Published online December 3, 2012

https://doi.org/10.1007/s10059-013-2271-3

© The Korean Society for Molecular and Cellular Biology

Expression and Function of the Testis-Predominant Protein LYAR in Mice

Boyeon Lee, Sora Jin, Heejin Choi, Jun Tae Kwon, Jihye Kim, Juri Jeong, Yong-il Kwon, and Chunghee Cho

School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Korea, Department of Obstetrics and Gynecology, Kangdong Sacred Heart Hospital, Hallym University College of Medicine, Seoul, Korea

Received: October 17, 2012; Revised: November 13, 2012; Accepted: November 14, 2012

Abstract

Mammalian spermatogenesis is a complex process involving an intrinsic genetic program of germ cell-specific and -predominant genes. In the present study, we analyzed the Ly-1 reactive clone (Lyar) gene in the mouse. Lyar, which is known to be expressed abundantly in the testis, encodes a nucleolar protein that contains a LYAR-type C2HC zinc finger motif and three nuclear localization signals. We herein confirmed that Lyar is expressed predominantly in the testis, and further showed that this expression is specific to germ cells. Protein analyses with an anti-LYAR antibody demonstrated that the LYAR protein is present in spermatocytes and spermatids, but not in sperm. To assess the functional role of LYAR in vivo, we used a genetrap mutagenesis approach to establish a LYAR-null mouse model. Lyar mutant mice were born live and developed normally. Male mutant mice lacking LYAR were fully fertile and showed intact spermatogenesis. Taken together, our results demonstrate that LYAR is strongly preferred in male germ cells, but has a dispensable role in spermatogenesis and fertility.

Keywords gene-trap, LYAR, nucleolar protein, spermatogenesis, testis

Article

Research Article

Mol. Cells 2013; 35(1): 54-60

Published online January 31, 2013 https://doi.org/10.1007/s10059-013-2271-3

Copyright © The Korean Society for Molecular and Cellular Biology.

Expression and Function of the Testis-Predominant Protein LYAR in Mice

Boyeon Lee, Sora Jin, Heejin Choi, Jun Tae Kwon, Jihye Kim, Juri Jeong, Yong-il Kwon, and Chunghee Cho

School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, Korea, Department of Obstetrics and Gynecology, Kangdong Sacred Heart Hospital, Hallym University College of Medicine, Seoul, Korea

Received: October 17, 2012; Revised: November 13, 2012; Accepted: November 14, 2012

Abstract

Mammalian spermatogenesis is a complex process involving an intrinsic genetic program of germ cell-specific and -predominant genes. In the present study, we analyzed the Ly-1 reactive clone (Lyar) gene in the mouse. Lyar, which is known to be expressed abundantly in the testis, encodes a nucleolar protein that contains a LYAR-type C2HC zinc finger motif and three nuclear localization signals. We herein confirmed that Lyar is expressed predominantly in the testis, and further showed that this expression is specific to germ cells. Protein analyses with an anti-LYAR antibody demonstrated that the LYAR protein is present in spermatocytes and spermatids, but not in sperm. To assess the functional role of LYAR in vivo, we used a genetrap mutagenesis approach to establish a LYAR-null mouse model. Lyar mutant mice were born live and developed normally. Male mutant mice lacking LYAR were fully fertile and showed intact spermatogenesis. Taken together, our results demonstrate that LYAR is strongly preferred in male germ cells, but has a dispensable role in spermatogenesis and fertility.

Keywords: gene-trap, LYAR, nucleolar protein, spermatogenesis, testis

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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