The male sterility and histoincompatibility ( mshi) mutation in mice is a natural variant of microtubule-associated protein 7 ( Mtap7)
Males homozygous for the mouse male sterility and histoincompatibility ( mshi) mutation exhibit small testes and produce no sperm. In addition, mshi generates an “antigen-loss” histoincompatibility barrier, such that homozygous mutants reject skin grafts from wild type co-isogenic BALB/cByJ donors....
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| Veröffentlicht in: | Molecular genetics and metabolism 2009-06, Vol.97 (2), p.155-162 |
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| creator | Magnan, D.R. Spacek, D.V. Ye, N. Lu, Y.-C. King, T.R. |
| description | Males homozygous for the mouse male sterility and histoincompatibility (
mshi) mutation exhibit small testes and produce no sperm. In addition,
mshi generates an “antigen-loss” histoincompatibility barrier, such that homozygous mutants reject skin grafts from wild type co-isogenic BALB/cByJ donors. To facilitate the molecular characterization of the pleiotropic
mshi mutation, we genetically mapped
mshi into a 0.68 megabasepair region which contains fewer than 10 candidate genes. Complementation testing showed that one of these,
Mtap7, is disrupted in
mshi mice. Sequence analysis has revealed a 13 kilobasepair deletion in BALB/cByJ-
mshi/J mice that begins in Intron 10–11 of
Mtap7, and ends less than 2000 base pairs downstream of the wild type gene. Analysis of the mutant cDNA predicts that
Mtap7
mshi
encodes a 457 amino acid protein, the first 423 of which are identical to wild type, and the last 34 of which are due to aberrant mRNA splicing with two cryptic exons in the
Mtap7 to
P04Rik intergenic region. This molecular assignment for the
mshi mutation further supports an essential role for microtubule stabilization in spermatogenesis and indicates a new role in allograft transplantation. |
| doi_str_mv | 10.1016/j.ymgme.2009.02.010 |
| format | Article |
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mshi) mutation exhibit small testes and produce no sperm. In addition,
mshi generates an “antigen-loss” histoincompatibility barrier, such that homozygous mutants reject skin grafts from wild type co-isogenic BALB/cByJ donors. To facilitate the molecular characterization of the pleiotropic
mshi mutation, we genetically mapped
mshi into a 0.68 megabasepair region which contains fewer than 10 candidate genes. Complementation testing showed that one of these,
Mtap7, is disrupted in
mshi mice. Sequence analysis has revealed a 13 kilobasepair deletion in BALB/cByJ-
mshi/J mice that begins in Intron 10–11 of
Mtap7, and ends less than 2000 base pairs downstream of the wild type gene. Analysis of the mutant cDNA predicts that
Mtap7
mshi
encodes a 457 amino acid protein, the first 423 of which are identical to wild type, and the last 34 of which are due to aberrant mRNA splicing with two cryptic exons in the
Mtap7 to
P04Rik intergenic region. This molecular assignment for the
mshi mutation further supports an essential role for microtubule stabilization in spermatogenesis and indicates a new role in allograft transplantation.</description><identifier>ISSN: 1096-7192</identifier><identifier>EISSN: 1096-7206</identifier><identifier>DOI: 10.1016/j.ymgme.2009.02.010</identifier><identifier>PMID: 19329343</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Base Sequence ; Chromosome Mapping ; Complementation ; Complementation testing ; DNA Mutational Analysis ; E-MAP-115 ; Genetic Complementation Test ; Histocompatibility - genetics ; Infertility, Male - genetics ; Male ; Mice ; Mice, Mutant Strains ; Microtubule-Associated Proteins - genetics ; Positional cloning ; Spermatogenesis ; Spermatogenesis - genetics</subject><ispartof>Molecular genetics and metabolism, 2009-06, Vol.97 (2), p.155-162</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-b560356601e34a98da5e468cb99f2040360e08b54a91d07bd988d13bb2bfa6233</citedby><cites>FETCH-LOGICAL-c488t-b560356601e34a98da5e468cb99f2040360e08b54a91d07bd988d13bb2bfa6233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ymgme.2009.02.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19329343$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Magnan, D.R.</creatorcontrib><creatorcontrib>Spacek, D.V.</creatorcontrib><creatorcontrib>Ye, N.</creatorcontrib><creatorcontrib>Lu, Y.-C.</creatorcontrib><creatorcontrib>King, T.R.</creatorcontrib><title>The male sterility and histoincompatibility ( mshi) mutation in mice is a natural variant of microtubule-associated protein 7 ( Mtap7)</title><title>Molecular genetics and metabolism</title><addtitle>Mol Genet Metab</addtitle><description>Males homozygous for the mouse male sterility and histoincompatibility (
mshi) mutation exhibit small testes and produce no sperm. In addition,
mshi generates an “antigen-loss” histoincompatibility barrier, such that homozygous mutants reject skin grafts from wild type co-isogenic BALB/cByJ donors. To facilitate the molecular characterization of the pleiotropic
mshi mutation, we genetically mapped
mshi into a 0.68 megabasepair region which contains fewer than 10 candidate genes. Complementation testing showed that one of these,
Mtap7, is disrupted in
mshi mice. Sequence analysis has revealed a 13 kilobasepair deletion in BALB/cByJ-
mshi/J mice that begins in Intron 10–11 of
Mtap7, and ends less than 2000 base pairs downstream of the wild type gene. Analysis of the mutant cDNA predicts that
Mtap7
mshi
encodes a 457 amino acid protein, the first 423 of which are identical to wild type, and the last 34 of which are due to aberrant mRNA splicing with two cryptic exons in the
Mtap7 to
P04Rik intergenic region. This molecular assignment for the
mshi mutation further supports an essential role for microtubule stabilization in spermatogenesis and indicates a new role in allograft transplantation.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Chromosome Mapping</subject><subject>Complementation</subject><subject>Complementation testing</subject><subject>DNA Mutational Analysis</subject><subject>E-MAP-115</subject><subject>Genetic Complementation Test</subject><subject>Histocompatibility - genetics</subject><subject>Infertility, Male - genetics</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Positional cloning</subject><subject>Spermatogenesis</subject><subject>Spermatogenesis - genetics</subject><issn>1096-7192</issn><issn>1096-7206</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUcmO1DAQjRCIWeALkJBPiDkklO3EiQ8goREDSIO4DGfLTirTbsV2iJ2W-gf4btx0s13gVKV6i8v1iuIZhYoCFa-21d7dO6wYgKyAVUDhQXFOQYqyZSAe_uypZGfFRYxbAEobWT8uzqjkTPKanxff7jZInJ6QxISLnWzaE-0HsrExBev74GadrDkCL4mLG3tF3JryMHhiPXG2R2Ij0cTrtC56Iju9WO0TCeMBXEJazTphqWMMvdUJBzLnIWZtmx0_JT23V0-KR6OeIj491cviy827u-sP5e3n9x-v396Wfd11qTSNAN4IARR5rWU36AZr0fVGypFBDVwAQmeajNEBWjPIrhsoN4aZUQvG-WXx5ug7r8bh0KNPeWU1L9bpZa-CtupvxNuNug87xUQHdSuzwYuTwRK-rhiTcjb2OE3aY1ijEi1jNTTtf4kMKG_rjmYiPxLzqWJccPy1DQV1CFpt1Y-g1SFoBUzloLPq-Z8f-a05JZsJr48EzOfcWVxU7C36Hge7YJ_UEOw_H_gO7Ey8xg</recordid><startdate>20090601</startdate><enddate>20090601</enddate><creator>Magnan, D.R.</creator><creator>Spacek, D.V.</creator><creator>Ye, N.</creator><creator>Lu, Y.-C.</creator><creator>King, T.R.</creator><general>Elsevier Inc</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>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090601</creationdate><title>The male sterility and histoincompatibility ( mshi) mutation in mice is a natural variant of microtubule-associated protein 7 ( Mtap7)</title><author>Magnan, D.R. ; Spacek, D.V. ; Ye, N. ; Lu, Y.-C. ; King, T.R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-b560356601e34a98da5e468cb99f2040360e08b54a91d07bd988d13bb2bfa6233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Chromosome Mapping</topic><topic>Complementation</topic><topic>Complementation testing</topic><topic>DNA Mutational Analysis</topic><topic>E-MAP-115</topic><topic>Genetic Complementation Test</topic><topic>Histocompatibility - genetics</topic><topic>Infertility, Male - genetics</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Microtubule-Associated Proteins - genetics</topic><topic>Positional cloning</topic><topic>Spermatogenesis</topic><topic>Spermatogenesis - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Magnan, D.R.</creatorcontrib><creatorcontrib>Spacek, D.V.</creatorcontrib><creatorcontrib>Ye, N.</creatorcontrib><creatorcontrib>Lu, Y.-C.</creatorcontrib><creatorcontrib>King, T.R.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular genetics and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Magnan, D.R.</au><au>Spacek, D.V.</au><au>Ye, N.</au><au>Lu, Y.-C.</au><au>King, T.R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The male sterility and histoincompatibility ( mshi) mutation in mice is a natural variant of microtubule-associated protein 7 ( Mtap7)</atitle><jtitle>Molecular genetics and metabolism</jtitle><addtitle>Mol Genet Metab</addtitle><date>2009-06-01</date><risdate>2009</risdate><volume>97</volume><issue>2</issue><spage>155</spage><epage>162</epage><pages>155-162</pages><issn>1096-7192</issn><eissn>1096-7206</eissn><abstract>Males homozygous for the mouse male sterility and histoincompatibility (
mshi) mutation exhibit small testes and produce no sperm. In addition,
mshi generates an “antigen-loss” histoincompatibility barrier, such that homozygous mutants reject skin grafts from wild type co-isogenic BALB/cByJ donors. To facilitate the molecular characterization of the pleiotropic
mshi mutation, we genetically mapped
mshi into a 0.68 megabasepair region which contains fewer than 10 candidate genes. Complementation testing showed that one of these,
Mtap7, is disrupted in
mshi mice. Sequence analysis has revealed a 13 kilobasepair deletion in BALB/cByJ-
mshi/J mice that begins in Intron 10–11 of
Mtap7, and ends less than 2000 base pairs downstream of the wild type gene. Analysis of the mutant cDNA predicts that
Mtap7
mshi
encodes a 457 amino acid protein, the first 423 of which are identical to wild type, and the last 34 of which are due to aberrant mRNA splicing with two cryptic exons in the
Mtap7 to
P04Rik intergenic region. This molecular assignment for the
mshi mutation further supports an essential role for microtubule stabilization in spermatogenesis and indicates a new role in allograft transplantation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19329343</pmid><doi>10.1016/j.ymgme.2009.02.010</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Molecular genetics and metabolism, 2009-06, Vol.97 (2), p.155-162 |
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| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Base Sequence Chromosome Mapping Complementation Complementation testing DNA Mutational Analysis E-MAP-115 Genetic Complementation Test Histocompatibility - genetics Infertility, Male - genetics Male Mice Mice, Mutant Strains Microtubule-Associated Proteins - genetics Positional cloning Spermatogenesis Spermatogenesis - genetics |
| title | The male sterility and histoincompatibility ( mshi) mutation in mice is a natural variant of microtubule-associated protein 7 ( Mtap7) |
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