Cryptorchidism and infertility in rats with targeted disruption of the Adamts16 locus
A Disintegrin And Metalloproteinase with ThromboSpondin motifs16 (ADAMTS-16) is a member of a family of metalloproteinases. Using a novel zinc-finger nuclease based gene-edited rat model harboring a targeted mutation of the Adamts16 locus, we previously reported this gene to be linked to blood press...
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| creator | Abdul-Majeed, Shakila Mell, Blair Nauli, Surya M Joe, Bina |
| description | A Disintegrin And Metalloproteinase with ThromboSpondin motifs16 (ADAMTS-16) is a member of a family of metalloproteinases. Using a novel zinc-finger nuclease based gene-edited rat model harboring a targeted mutation of the Adamts16 locus, we previously reported this gene to be linked to blood pressure regulation. Here we document our observation with this model that Adamts16 is essential for normal development of the testis. Absence of Adamts16 in the homozygous Adamts16mutant males resulted in cryptorchidism and male sterility. Heterozygous Adamts16mutant males were normal, indicating that this is a recessive trait. Testes of homozygous Adamts16mutant males were significantly smaller with significant histological changes associated with the lack of sperm production. Temporal histological assessments of the testis demonstrated that the seminiferous tubules did not support active spermatogenesis, but progressively lost germ cells, accumulated vacuoles and did not have any sperm. These observations, taken together with our previous report of renal abnormalities observed with the same Adamts16mutant rats, suggest an important mechanistic link between Adamts16 and the functioning of the male genitourinary system. |
| doi_str_mv | 10.1371/journal.pone.0100967 |
| format | Article |
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Using a novel zinc-finger nuclease based gene-edited rat model harboring a targeted mutation of the Adamts16 locus, we previously reported this gene to be linked to blood pressure regulation. Here we document our observation with this model that Adamts16 is essential for normal development of the testis. Absence of Adamts16 in the homozygous Adamts16mutant males resulted in cryptorchidism and male sterility. Heterozygous Adamts16mutant males were normal, indicating that this is a recessive trait. Testes of homozygous Adamts16mutant males were significantly smaller with significant histological changes associated with the lack of sperm production. Temporal histological assessments of the testis demonstrated that the seminiferous tubules did not support active spermatogenesis, but progressively lost germ cells, accumulated vacuoles and did not have any sperm. These observations, taken together with our previous report of renal abnormalities observed with the same Adamts16mutant rats, suggest an important mechanistic link between Adamts16 and the functioning of the male genitourinary system.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0100967</identifier><identifier>PMID: 24983376</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; ADAM protein ; ADAM Proteins - genetics ; Alcohol ; Animals ; Antigens ; Biology and Life Sciences ; Blood pressure ; Cryptorchidism ; Cryptorchidism - enzymology ; Cryptorchidism - genetics ; Cryptorchidism - pathology ; Ethanol ; Extracellular matrix ; Gene expression ; Genetic Loci ; Genetic modification ; Genitourinary system ; Genomics ; Germ cells ; Hypertension ; Infertility ; Infertility, Male - enzymology ; Infertility, Male - genetics ; Infertility, Male - pathology ; Kidney - abnormalities ; Life sciences ; Loci ; Male ; Male sterility ; Males ; Medicine and Health Sciences ; Mutation ; Nuclease ; Pharmacology ; Physiology ; Precision medicine ; Proteins ; Rats ; Rodents ; Spermatogenesis ; Sterility ; Testes ; Thrombospondin ; Tubules ; Undescended testes ; Urogenital system ; Vacuoles ; Zinc ; Zinc finger proteins</subject><ispartof>PloS one, 2014-07, Vol.9 (7), p.e100967-e100967</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Abdul-Majeed et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Using a novel zinc-finger nuclease based gene-edited rat model harboring a targeted mutation of the Adamts16 locus, we previously reported this gene to be linked to blood pressure regulation. Here we document our observation with this model that Adamts16 is essential for normal development of the testis. Absence of Adamts16 in the homozygous Adamts16mutant males resulted in cryptorchidism and male sterility. Heterozygous Adamts16mutant males were normal, indicating that this is a recessive trait. Testes of homozygous Adamts16mutant males were significantly smaller with significant histological changes associated with the lack of sperm production. Temporal histological assessments of the testis demonstrated that the seminiferous tubules did not support active spermatogenesis, but progressively lost germ cells, accumulated vacuoles and did not have any sperm. These observations, taken together with our previous report of renal abnormalities observed with the same Adamts16mutant rats, suggest an important mechanistic link between Adamts16 and the functioning of the male genitourinary system.</description><subject>Abnormalities</subject><subject>ADAM protein</subject><subject>ADAM Proteins - genetics</subject><subject>Alcohol</subject><subject>Animals</subject><subject>Antigens</subject><subject>Biology and Life Sciences</subject><subject>Blood pressure</subject><subject>Cryptorchidism</subject><subject>Cryptorchidism - enzymology</subject><subject>Cryptorchidism - genetics</subject><subject>Cryptorchidism - pathology</subject><subject>Ethanol</subject><subject>Extracellular matrix</subject><subject>Gene expression</subject><subject>Genetic Loci</subject><subject>Genetic modification</subject><subject>Genitourinary system</subject><subject>Genomics</subject><subject>Germ cells</subject><subject>Hypertension</subject><subject>Infertility</subject><subject>Infertility, Male - enzymology</subject><subject>Infertility, Male - genetics</subject><subject>Infertility, Male - pathology</subject><subject>Kidney - abnormalities</subject><subject>Life sciences</subject><subject>Loci</subject><subject>Male</subject><subject>Male sterility</subject><subject>Males</subject><subject>Medicine and Health Sciences</subject><subject>Mutation</subject><subject>Nuclease</subject><subject>Pharmacology</subject><subject>Physiology</subject><subject>Precision medicine</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Spermatogenesis</subject><subject>Sterility</subject><subject>Testes</subject><subject>Thrombospondin</subject><subject>Tubules</subject><subject>Undescended testes</subject><subject>Urogenital system</subject><subject>Vacuoles</subject><subject>Zinc</subject><subject>Zinc finger proteins</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLgujFjPlOeyMMgx8DCwvqehvSJJ1mSZsxSdX592ac7jKVvZBcJJw85z05J29RPIdgCTGH7278GAbpljs_mCWAANSMPyjOYY3RgiGAH56cz4onMd4AQHHF2OPiDJG6wpiz8-J6Hfa75IPqrLaxL-WgSzu0JiTrbNrncxlkiuUvm7oyybA1yegyo2HcJeuH0rdl6ky50rJPEbLSeTXGp8WjVrponk37RXH98cO39efF5dWnzXp1uVCsRmmhGlxTrYyEjGOjTYt0pRqOUWMgQJphRZtW8ZoBrEjFaKsk1hpAZBClVdXii-LlUXfnfBTTRKKAlCBAAOEkE5sjob28Ebtgexn2wksr_gZ82AqZe1XOCFrVrWQ0F64QoY2uicZEA8RMm3etstb7qdrY9Ca_e0hBupno_Gawndj6n4IAzjlDWeDNJBD8j9HEJHoblXFODsaPx3cziqoaZPTVP-j93U3UVuYG8r_5XFcdRMWKQMY4r-Gh7PIeKi9tequyfVqb47OEt7OEzCTzO23lGKPYfP3y_-zV9zn7-oTtjHSpi96NByPFOUiOoAo-xmDauyFDIA7uv52GOLhfTO7PaS9OP-gu6dbu-A-Xrf_L</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Abdul-Majeed, Shakila</creator><creator>Mell, Blair</creator><creator>Nauli, Surya M</creator><creator>Joe, Bina</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140701</creationdate><title>Cryptorchidism and infertility in rats with targeted disruption of the Adamts16 locus</title><author>Abdul-Majeed, Shakila ; Mell, Blair ; Nauli, Surya M ; Joe, Bina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-cb395dcea1673edef2d8cb732be102d63c5bfc79603c4865fca3dd012e25588f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Abnormalities</topic><topic>ADAM protein</topic><topic>ADAM Proteins - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abdul-Majeed, Shakila</au><au>Mell, Blair</au><au>Nauli, Surya M</au><au>Joe, Bina</au><au>Singh, Shree Ram</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cryptorchidism and infertility in rats with targeted disruption of the Adamts16 locus</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>9</volume><issue>7</issue><spage>e100967</spage><epage>e100967</epage><pages>e100967-e100967</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>A Disintegrin And Metalloproteinase with ThromboSpondin motifs16 (ADAMTS-16) is a member of a family of metalloproteinases. Using a novel zinc-finger nuclease based gene-edited rat model harboring a targeted mutation of the Adamts16 locus, we previously reported this gene to be linked to blood pressure regulation. Here we document our observation with this model that Adamts16 is essential for normal development of the testis. Absence of Adamts16 in the homozygous Adamts16mutant males resulted in cryptorchidism and male sterility. Heterozygous Adamts16mutant males were normal, indicating that this is a recessive trait. Testes of homozygous Adamts16mutant males were significantly smaller with significant histological changes associated with the lack of sperm production. Temporal histological assessments of the testis demonstrated that the seminiferous tubules did not support active spermatogenesis, but progressively lost germ cells, accumulated vacuoles and did not have any sperm. These observations, taken together with our previous report of renal abnormalities observed with the same Adamts16mutant rats, suggest an important mechanistic link between Adamts16 and the functioning of the male genitourinary system.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24983376</pmid><doi>10.1371/journal.pone.0100967</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Abnormalities ADAM protein ADAM Proteins - genetics Alcohol Animals Antigens Biology and Life Sciences Blood pressure Cryptorchidism Cryptorchidism - enzymology Cryptorchidism - genetics Cryptorchidism - pathology Ethanol Extracellular matrix Gene expression Genetic Loci Genetic modification Genitourinary system Genomics Germ cells Hypertension Infertility Infertility, Male - enzymology Infertility, Male - genetics Infertility, Male - pathology Kidney - abnormalities Life sciences Loci Male Male sterility Males Medicine and Health Sciences Mutation Nuclease Pharmacology Physiology Precision medicine Proteins Rats Rodents Spermatogenesis Sterility Testes Thrombospondin Tubules Undescended testes Urogenital system Vacuoles Zinc Zinc finger proteins |
| title | Cryptorchidism and infertility in rats with targeted disruption of the Adamts16 locus |
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