Using a mouse model in which Dot1l is knocked-out (KO) in postnatal male germ cells, we found that Dot1l-KO sperm chromatin is less compact and has an abnormal content.
First-pass extracted concept
Dot1l knockout in postnatal male germ cells
Candidate: concept label1 source documents3 linked claims
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Aliases
Dot1l-KO, mouse model in which Dot1l is knocked-out (KO) in postnatal male germ cells
Evidence Snippets
Supporting Sources
Linked Claims
Proteomic and transcriptomic analyses of spermatids indicate that Dot1l knockout modifies chromatin prior to histone removal and deregulates genes involved in flagellum formation and apoptosis during spermatid differentiation.
Quoted textsource-backed
Proteomic and transcriptomic analyses performed on spermatids reveal that Dot1l-KO modifies the chromatin prior to histone removal and leads to the deregulation of genes involved in flagellum formation and apoptosis during spermatid differentiation.
Dot1l knockout causes spermatozoa to have less compact heads and reduced motility, resulting in impaired fertility.
Quoted textsource-backed
As a consequence of these chromatin and gene expression defects, Dot1l-KO spermatozoa have less compact heads and are less motile, which results in impaired fertility.
Dot1l knockout in postnatal male germ cells produces sperm chromatin that is less compact and has abnormal content including transition proteins, immature protamine 2 forms, and higher histone levels.
Quoted textsource-backed
Using a mouse model in which Dot1l is knocked-out (KO) in postnatal male germ cells, we found that Dot1l-KO sperm chromatin is less compact and has an abnormal content, characterized by the presence of transition proteins, immature protamine 2 forms and a higher level of histones.