MNS1 is essential for spermiogenesis and motile ciliary functions in mice.

During spermiogenesis, haploid round spermatids undergo dramatic cell differentiation and morphogenesis to give rise to mature spermatozoa for fertilization, including nuclear elongation, chromatin remodeling, acrosome formation, and development of flagella. The molecular mechanisms underlining thes...

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Main Authors: Jian Zhou, Fang Yang, N Adrian Leu, P Jeremy Wang
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS Genetics
Online Access:http://europepmc.org/articles/PMC3291534?pdf=render
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spelling doaj-e2164d1f128443dea69297c17e77a7832020-11-24T22:20:29ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042012-01-0183e100251610.1371/journal.pgen.1002516MNS1 is essential for spermiogenesis and motile ciliary functions in mice.Jian ZhouFang YangN Adrian LeuP Jeremy WangDuring spermiogenesis, haploid round spermatids undergo dramatic cell differentiation and morphogenesis to give rise to mature spermatozoa for fertilization, including nuclear elongation, chromatin remodeling, acrosome formation, and development of flagella. The molecular mechanisms underlining these fundamental processes remain poorly understood. Here, we report that MNS1, a coiled-coil protein of unknown function, is essential for spermiogenesis. We find that MNS1 is expressed in the germ cells in the testes and localizes to sperm flagella in a detergent-resistant manner, indicating that it is an integral component of flagella. MNS1-deficient males are sterile, as they exhibit a sharp reduction in sperm production and the remnant sperm are immotile with abnormal short tails. In MNS1-deficient sperm flagella, the characteristic arrangement of "9+2" microtubules and outer dense fibers are completely disrupted. In addition, MNS1-deficient mice display situs inversus and hydrocephalus. MNS1-deficient tracheal motile cilia lack some outer dynein arms in the axoneme. Moreover, MNS1 monomers interact with each other and are able to form polymers in cultured somatic cells. These results demonstrate that MNS1 is essential for spermiogenesis, the assembly of sperm flagella, and motile ciliary functions.http://europepmc.org/articles/PMC3291534?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Jian Zhou
Fang Yang
N Adrian Leu
P Jeremy Wang
spellingShingle Jian Zhou
Fang Yang
N Adrian Leu
P Jeremy Wang
MNS1 is essential for spermiogenesis and motile ciliary functions in mice.
PLoS Genetics
author_facet Jian Zhou
Fang Yang
N Adrian Leu
P Jeremy Wang
author_sort Jian Zhou
title MNS1 is essential for spermiogenesis and motile ciliary functions in mice.
title_short MNS1 is essential for spermiogenesis and motile ciliary functions in mice.
title_full MNS1 is essential for spermiogenesis and motile ciliary functions in mice.
title_fullStr MNS1 is essential for spermiogenesis and motile ciliary functions in mice.
title_full_unstemmed MNS1 is essential for spermiogenesis and motile ciliary functions in mice.
title_sort mns1 is essential for spermiogenesis and motile ciliary functions in mice.
publisher Public Library of Science (PLoS)
series PLoS Genetics
issn 1553-7390
1553-7404
publishDate 2012-01-01
description During spermiogenesis, haploid round spermatids undergo dramatic cell differentiation and morphogenesis to give rise to mature spermatozoa for fertilization, including nuclear elongation, chromatin remodeling, acrosome formation, and development of flagella. The molecular mechanisms underlining these fundamental processes remain poorly understood. Here, we report that MNS1, a coiled-coil protein of unknown function, is essential for spermiogenesis. We find that MNS1 is expressed in the germ cells in the testes and localizes to sperm flagella in a detergent-resistant manner, indicating that it is an integral component of flagella. MNS1-deficient males are sterile, as they exhibit a sharp reduction in sperm production and the remnant sperm are immotile with abnormal short tails. In MNS1-deficient sperm flagella, the characteristic arrangement of "9+2" microtubules and outer dense fibers are completely disrupted. In addition, MNS1-deficient mice display situs inversus and hydrocephalus. MNS1-deficient tracheal motile cilia lack some outer dynein arms in the axoneme. Moreover, MNS1 monomers interact with each other and are able to form polymers in cultured somatic cells. These results demonstrate that MNS1 is essential for spermiogenesis, the assembly of sperm flagella, and motile ciliary functions.
url http://europepmc.org/articles/PMC3291534?pdf=render
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