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TAp73 is required for spermatogenesis and the maintenance of male fertility.

The generation of viable sperm proceeds through a series of coordinated steps, including germ cell self-renewal, meiotic recombination, and terminal differentiation into functional spermatozoa. The p53 family of transcription factors, including p53, p63, and p73, are critical for many physiological... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America February 4, 2014, Vol.111(5), pp.1843-1848
Main Author: Inoue, Satoshi
Other Authors: Tomasini, Richard , Rufini, Alessandro , Elia, Andrew J , Agostini, Massimiliano , Amelio, Ivano , Cescon, Dave , Dinsdale, David , Zhou, Lily , Harris, Isaac S , Lac, Sophie , Silvester, Jennifer , Li, Wanda Y , Sasaki, Masato , Haight, Jillian , Brüstle, Anne , Wakeham, Andrew , Mckerlie, Colin , Jurisicova, Andrea , Melino, Gerry , Mak, Tak W
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1323416111
Link: http://search.proquest.com/docview/1499115504/?pq-origsite=primo
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title: TAp73 is required for spermatogenesis and the maintenance of male fertility.
format: Article
creator:
  • Inoue, Satoshi
  • Tomasini, Richard
  • Rufini, Alessandro
  • Elia, Andrew J
  • Agostini, Massimiliano
  • Amelio, Ivano
  • Cescon, Dave
  • Dinsdale, David
  • Zhou, Lily
  • Harris, Isaac S
  • Lac, Sophie
  • Silvester, Jennifer
  • Li, Wanda Y
  • Sasaki, Masato
  • Haight, Jillian
  • Brüstle, Anne
  • Wakeham, Andrew
  • Mckerlie, Colin
  • Jurisicova, Andrea
  • Melino, Gerry
  • Mak, Tak W
subjects:
  • Adam Proteins–Genetics
  • Adam17 Protein–Metabolism
  • Aging–Pathology
  • Animals–Genetics
  • Apoptosis–Genetics
  • Cell Count–Deficiency
  • Cell Proliferation–Metabolism
  • DNA Damage–Genetics
  • DNA-Binding Proteins–Blood
  • Female–Genetics
  • Fertility–Pathology
  • Gene Expression Regulation–Genetics
  • Humans–Metabolism
  • Infertility, Male–Deficiency
  • Male–Metabolism
  • Matrix Metalloproteinase 13–Genetics
  • Mice–Blood
  • Mice, Knockout–Genetics
  • Nuclear Proteins–Metabolism
  • Oxidative Stress–Genetics
  • Progesterone–Metabolism
  • RNA, Messenger–Pathology
  • Spermatogenesis–Metabolism
  • Spermatozoa–Pathology
  • Testis–Deficiency
  • Tumor Protein P73–Metabolism
  • Tumor Suppressor Proteins–Metabolism
  • DNA-Binding Proteins
  • Nuclear Proteins
  • RNA, Messenger
  • Trp73 Protein, Mouse
  • Tumor Protein P73
  • Tumor Suppressor Proteins
  • Delta Np73 Protein, Human
  • P73 Protein, Human
  • Progesterone
  • Adam Proteins
  • Matrix Metalloproteinase 13
  • Mmp13 Protein, Mouse
  • Adam17 Protein
  • Adam17 Protein, Human
  • Adam17 Protein, Mouse
  • Adam17
  • Mmp13
  • Serpin
  • Timp
ispartof: Proceedings of the National Academy of Sciences of the United States of America, February 4, 2014, Vol.111(5), pp.1843-1848
description: The generation of viable sperm proceeds through a series of coordinated steps, including germ cell self-renewal, meiotic recombination, and terminal differentiation into functional spermatozoa. The p53 family of transcription factors, including p53, p63, and p73, are critical for many physiological processes, including female fertility, but little is known about their functions in spermatogenesis. Here, we report that deficiency of the TAp73 isoform, but not p53 or [DELTA]Np73, results in male infertility because of severe impairment of spermatogenesis. Mice lacking TAp73 exhibited increased DNA damage and cell death in spermatogonia, disorganized apical ectoplasmic specialization, malformed spermatids, and marked hyperspermia. We demonstrated that TAp73 regulates the mRNA levels of crucial genes involved in germ stem/progenitor cells (CDKN2B), spermatid maturation/spermiogenesis (metalloproteinase and serine proteinase inhibitors), and steroidogenesis (CYP21A2 and progesterone receptor). These alterations of testicular histology and gene expression patterns were specific to TAp73 null mice and not features of mice lacking p53. Our work provides previously unidentified in vivo evidence that TAp73 has a unique role in spermatogenesis that ensures the maintenance of mitotic cells and normal spermiogenesis. These results may have implications for the diagnosis and management of human male infertility. ADAM17 | MMP13 | Serpin | Timp www.pnas.org/cgi/doi/10.1073/pnas.1323416111
language: eng
source:
identifier: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1323416111
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleTAp73 is required for spermatogenesis and the maintenance of male fertility.
creatorInoue, Satoshi ; Tomasini, Richard ; Rufini, Alessandro ; Elia, Andrew J ; Agostini, Massimiliano ; Amelio, Ivano ; Cescon, Dave ; Dinsdale, David ; Zhou, Lily ; Harris, Isaac S ; Lac, Sophie ; Silvester, Jennifer ; Li, Wanda Y ; Sasaki, Masato ; Haight, Jillian ; Brüstle, Anne ; Wakeham, Andrew ; Mckerlie, Colin ; Jurisicova, Andrea ; Melino, Gerry ; Mak, Tak W
contributorInoue, Satoshi (correspondence author) ; Inoue, Satoshi (record owner)
ispartofProceedings of the National Academy of Sciences of the United States of America, February 4, 2014, Vol.111(5), pp.1843-1848
identifierE-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1323416111
subjectAdam Proteins–Genetics ; Adam17 Protein–Metabolism ; Aging–Pathology ; Animals–Genetics ; Apoptosis–Genetics ; Cell Count–Deficiency ; Cell Proliferation–Metabolism ; DNA Damage–Genetics ; DNA-Binding Proteins–Blood ; Female–Genetics ; Fertility–Pathology ; Gene Expression Regulation–Genetics ; Humans–Metabolism ; Infertility, Male–Deficiency ; Male–Metabolism ; Matrix Metalloproteinase 13–Genetics ; Mice–Blood ; Mice, Knockout–Genetics ; Nuclear Proteins–Metabolism ; Oxidative Stress–Genetics ; Progesterone–Metabolism ; RNA, Messenger–Pathology ; Spermatogenesis–Metabolism ; Spermatozoa–Pathology ; Testis–Deficiency ; Tumor Protein P73–Metabolism ; Tumor Suppressor Proteins–Metabolism ; DNA-Binding Proteins ; Nuclear Proteins ; RNA, Messenger ; Trp73 Protein, Mouse ; Tumor Protein P73 ; Tumor Suppressor Proteins ; Delta Np73 Protein, Human ; P73 Protein, Human ; Progesterone ; Adam Proteins ; Matrix Metalloproteinase 13 ; Mmp13 Protein, Mouse ; Adam17 Protein ; Adam17 Protein, Human ; Adam17 Protein, Mouse ; Adam17 ; Mmp13 ; Serpin ; Timp
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descriptionThe generation of viable sperm proceeds through a series of coordinated steps, including germ cell self-renewal, meiotic recombination, and terminal differentiation into functional spermatozoa. The p53 family of transcription factors, including p53, p63, and p73, are critical for many physiological processes, including female fertility, but little is known about their functions in spermatogenesis. Here, we report that deficiency of the TAp73 isoform, but not p53 or [DELTA]Np73, results in male infertility because of severe impairment of spermatogenesis. Mice lacking TAp73 exhibited increased DNA damage and cell death in spermatogonia, disorganized apical ectoplasmic specialization, malformed spermatids, and marked hyperspermia. We demonstrated that TAp73 regulates the mRNA levels of crucial genes involved in germ stem/progenitor cells (CDKN2B), spermatid maturation/spermiogenesis (metalloproteinase and serine proteinase inhibitors), and steroidogenesis (CYP21A2 and progesterone receptor). These alterations of testicular histology and gene expression patterns were specific to TAp73 null mice and not features of mice lacking p53. Our work provides previously unidentified in vivo evidence that TAp73 has a unique role in spermatogenesis that ensures the maintenance of mitotic cells and normal spermiogenesis. These results may have implications for the diagnosis and management of human male infertility. ADAM17 | MMP13 | Serpin | Timp www.pnas.org/cgi/doi/10.1073/pnas.1323416111
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19Melino, Gerry
20Mak, Tak W
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titleTAp73 is required for spermatogenesis and the maintenance of male fertility.
authorInoue, Satoshi ; Tomasini, Richard ; Rufini, Alessandro ; Elia, Andrew J ; Agostini, Massimiliano ; Amelio, Ivano ; Cescon, Dave ; Dinsdale, David ; Zhou, Lily ; Harris, Isaac S ; Lac, Sophie ; Silvester, Jennifer ; Li, Wanda Y ; Sasaki, Masato ; Haight, Jillian ; Brüstle, Anne ; Wakeham, Andrew ; Mckerlie,...
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