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dc.contributor.authorZhang, Zhengang
dc.contributor.authorLi, Wei
dc.contributor.authorZhang, Yong
dc.contributor.authorZhang, Ling
dc.contributor.authorTeves, Maria E.
dc.contributor.authorLiu, Hong
dc.contributor.authorStrauss, Jerome F. 3rd
dc.contributor.authorPazour, Gregory J.
dc.contributor.authorFoster, James A.
dc.contributor.authorHess, Rex A.
dc.contributor.authorZhang, Zhibing
dc.date2022-08-11T08:08:22.000
dc.date.accessioned2022-08-23T15:52:24Z
dc.date.available2022-08-23T15:52:24Z
dc.date.issued2016-11-15
dc.date.submitted2017-06-30
dc.identifier.citationMol Biol Cell. 2016 Nov 15; 27(23): 3705–3716. doi: 10.1091/mbc.E16-05-0318. <a href="https://doi.org/10.1091/mbc.E16-05-0318">Link to article on publisher's site</a>
dc.identifier.issn1059-1524 (Linking)
dc.identifier.doi10.1091/mbc.E16-05-0318
dc.identifier.pmid27682589
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29128
dc.description.abstractIntraflagellar transport (IFT) is a conserved mechanism thought to be essential for the assembly and maintenance of cilia and flagella. However, little is known about its role in mammalian sperm flagella formation. To fill this gap, we disrupted the Ift20 gene in male germ cells. Homozygous mutant mice were infertile with significantly reduced sperm counts and motility. In addition, abnormally shaped elongating spermatid heads and bulbous round spermatids were found in the lumen of the seminiferous tubules. Electron microscopy revealed increased cytoplasmic vesicles, fiber-like structures, abnormal accumulation of mitochondria and a decrease in mature lysosomes. The few developed sperm had disrupted axonemes and some retained cytoplasmic lobe components on the flagella. ODF2 and SPAG16L, two sperm flagella proteins failed to be incorporated into sperm tails of the mutant mice, and in the germ cells, both were assembled into complexes with lighter density in the absence of IFT20. Disrupting IFT20 did not significantly change expression levels of IFT88, a component of IFT-B complex, and IFT140, a component of IFT-A complex. Even though the expression level of an autophagy core protein that associates with IFT20, ATG16, was reduced in the testis of the Ift20 mutant mice, expression levels of other major autophagy markers, including LC3 and ubiquitin were not changed. Our studies suggest that IFT20 is essential for male fertility and spermiogenesis in mice, and its major function is to transport cargo proteins for sperm flagella formation. It also appears to be involved in removing excess cytoplasmic components.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27682589&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rights© 2016 Zhang et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/
dc.subjectIFT20
dc.subjectmale fertility
dc.subjectspermiogenesis
dc.subjectmice
dc.subjectflagella
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectDevelopmental Biology
dc.subjectMolecular Biology
dc.titleIntraflagellar transport protein IFT20 is essential for male fertility and spermiogenesis in mice
dc.typeJournal Article
dc.source.journaltitleMolecular biology of the cell
dc.source.volume27
dc.source.issue23
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2356&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1353
dc.identifier.contextkey10382250
refterms.dateFOA2022-08-23T15:52:24Z
html.description.abstract<p>Intraflagellar transport (IFT) is a conserved mechanism thought to be essential for the assembly and maintenance of cilia and flagella. However, little is known about its role in mammalian sperm flagella formation. To fill this gap, we disrupted the Ift20 gene in male germ cells. Homozygous mutant mice were infertile with significantly reduced sperm counts and motility. In addition, abnormally shaped elongating spermatid heads and bulbous round spermatids were found in the lumen of the seminiferous tubules. Electron microscopy revealed increased cytoplasmic vesicles, fiber-like structures, abnormal accumulation of mitochondria and a decrease in mature lysosomes. The few developed sperm had disrupted axonemes and some retained cytoplasmic lobe components on the flagella. ODF2 and SPAG16L, two sperm flagella proteins failed to be incorporated into sperm tails of the mutant mice, and in the germ cells, both were assembled into complexes with lighter density in the absence of IFT20. Disrupting IFT20 did not significantly change expression levels of IFT88, a component of IFT-B complex, and IFT140, a component of IFT-A complex. Even though the expression level of an autophagy core protein that associates with IFT20, ATG16, was reduced in the testis of the Ift20 mutant mice, expression levels of other major autophagy markers, including LC3 and ubiquitin were not changed. Our studies suggest that IFT20 is essential for male fertility and spermiogenesis in mice, and its major function is to transport cargo proteins for sperm flagella formation. It also appears to be involved in removing excess cytoplasmic components.</p>
dc.identifier.submissionpathfaculty_pubs/1353
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages3705–3716


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© 2016 Zhang et al. This article is distributed by The American Society for Cell
Biology under license from the author(s). Two months after publication it is available
to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported
Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
Except where otherwise noted, this item's license is described as © 2016 Zhang et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).