UNC-52/Perlecan affects gonadal leader cell migrations in c. elegans hermaphrodites through alterations in growth factor signaling
The unc-52 gene of Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the...
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| Veröffentlicht in: | Developmental biology 2003-04, Vol.256 (1), p.174-187 |
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| creator | Merz, David C Alves, Georges Kawano, Takehiro Zheng, Hong Culotti, Joseph G |
| description | The
unc-52 gene of
Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These
unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of
unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecules, including EGL-17/FGF, UNC-129/TGF-β, DBL-1/TGF-β, and EGL-20/WNT. We propose that UNC-52 serves dual roles in
C. elegans larval development in the maintenance of muscle structure and the regulation of growth factor-like signaling pathways. |
| doi_str_mv | 10.1016/S0012-1606(03)00014-9 |
| format | Article |
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unc-52 gene of
Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These
unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of
unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecules, including EGL-17/FGF, UNC-129/TGF-β, DBL-1/TGF-β, and EGL-20/WNT. We propose that UNC-52 serves dual roles in
C. elegans larval development in the maintenance of muscle structure and the regulation of growth factor-like signaling pathways.</description><identifier>ISSN: 0012-1606</identifier><identifier>EISSN: 1095-564X</identifier><identifier>DOI: 10.1016/S0012-1606(03)00014-9</identifier><identifier>PMID: 12654300</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Animals, Genetically Modified ; C. elegans ; Caenorhabditis elegans - cytology ; Caenorhabditis elegans - genetics ; Caenorhabditis elegans - growth & development ; Caenorhabditis elegans - metabolism ; Caenorhabditis elegans Proteins - genetics ; Caenorhabditis elegans Proteins - metabolism ; Cell migrations ; Cell Movement - genetics ; Disorders of Sex Development ; Female ; Genes, Helminth ; Gonads - cytology ; Gonads - growth & development ; Gonads - metabolism ; Growth Substances - genetics ; Growth Substances - metabolism ; Helminth Proteins - genetics ; Helminth Proteins - metabolism ; Larva - cytology ; Larva - growth & development ; Larva - metabolism ; Male ; Membrane Proteins ; Muscles - metabolism ; Mutation ; Nerve Tissue Proteins ; Netrins ; Organogenesis ; Perlecan ; Phenotype ; Protein Tyrosine Phosphatases - genetics ; Proteoglycans - genetics ; Proteoglycans - metabolism ; Receptor-Like Protein Tyrosine Phosphatases ; Receptors, Cell Surface - genetics ; Receptors, Fibroblast Growth Factor - genetics ; Signal Transduction ; UNC-52</subject><ispartof>Developmental biology, 2003-04, Vol.256 (1), p.174-187</ispartof><rights>2003 Elsevier Science (USA)</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-b3adc4922b0587049c09c751094edfa9906b4e0c0ea666fa11618c46613c161e3</citedby><cites>FETCH-LOGICAL-c539t-b3adc4922b0587049c09c751094edfa9906b4e0c0ea666fa11618c46613c161e3</cites><orcidid>0000-0002-5548-0270</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0012160603000149$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12654300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00457505$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Merz, David C</creatorcontrib><creatorcontrib>Alves, Georges</creatorcontrib><creatorcontrib>Kawano, Takehiro</creatorcontrib><creatorcontrib>Zheng, Hong</creatorcontrib><creatorcontrib>Culotti, Joseph G</creatorcontrib><title>UNC-52/Perlecan affects gonadal leader cell migrations in c. elegans hermaphrodites through alterations in growth factor signaling</title><title>Developmental biology</title><addtitle>Dev Biol</addtitle><description>The
unc-52 gene of
Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These
unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of
unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecules, including EGL-17/FGF, UNC-129/TGF-β, DBL-1/TGF-β, and EGL-20/WNT. We propose that UNC-52 serves dual roles in
C. elegans larval development in the maintenance of muscle structure and the regulation of growth factor-like signaling pathways.</description><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>C. elegans</subject><subject>Caenorhabditis elegans - cytology</subject><subject>Caenorhabditis elegans - genetics</subject><subject>Caenorhabditis elegans - growth & development</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Caenorhabditis elegans Proteins - genetics</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Cell migrations</subject><subject>Cell Movement - genetics</subject><subject>Disorders of Sex Development</subject><subject>Female</subject><subject>Genes, Helminth</subject><subject>Gonads - cytology</subject><subject>Gonads - growth & development</subject><subject>Gonads - metabolism</subject><subject>Growth Substances - genetics</subject><subject>Growth Substances - metabolism</subject><subject>Helminth Proteins - genetics</subject><subject>Helminth Proteins - metabolism</subject><subject>Larva - cytology</subject><subject>Larva - growth & development</subject><subject>Larva - metabolism</subject><subject>Male</subject><subject>Membrane Proteins</subject><subject>Muscles - metabolism</subject><subject>Mutation</subject><subject>Nerve Tissue Proteins</subject><subject>Netrins</subject><subject>Organogenesis</subject><subject>Perlecan</subject><subject>Phenotype</subject><subject>Protein Tyrosine Phosphatases - genetics</subject><subject>Proteoglycans - genetics</subject><subject>Proteoglycans - metabolism</subject><subject>Receptor-Like Protein Tyrosine Phosphatases</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Fibroblast Growth Factor - genetics</subject><subject>Signal Transduction</subject><subject>UNC-52</subject><issn>0012-1606</issn><issn>1095-564X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQhS0EokvhJ4B8QvSQdhzHTnxC1YpSpBUgQSVulteZJEZOvNjZIq795TjdVeHWk2es73nG7xHymsE5AyYvvgGwsmAS5DvgZ5C7qlBPyIqBEoWQ1Y-nZPWAnJAXKf3MEG8a_pycsFKKigOsyN3N53UhyouvGD1aM1HTdWjnRPswmdZ46tG0GKlF7-no-mhmF6ZE3UTtOUWPvcndgHE0uyGG1s2Y6JyrfT9Q42f8T9DH8HseaGfsHCJNrp-Md1P_kjzrjE_46niekpurD9_X18Xmy8dP68tNYQVXc7HlprWVKsstiKaGSllQthb5vxW2nVEK5LZCsIBGStkZxiRrbCUl4zaXyE_J2eHdwXi9i2408Y8Oxunry41e7gAqUQsQtyyzbw_sLoZfe0yzHl1aPDAThn3SNV8sFM2jIGukgrosMygOoI0hpYjdwwoM9JKovk9UL3Fp4Po-Ua2y7s1xwH47YvtPdYwwA-8PAGbvbh1GnazDyWLrYk5St8E9MuIvdw-vyQ</recordid><startdate>20030401</startdate><enddate>20030401</enddate><creator>Merz, David C</creator><creator>Alves, Georges</creator><creator>Kawano, Takehiro</creator><creator>Zheng, Hong</creator><creator>Culotti, Joseph G</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-5548-0270</orcidid></search><sort><creationdate>20030401</creationdate><title>UNC-52/Perlecan affects gonadal leader cell migrations in c. elegans hermaphrodites through alterations in growth factor signaling</title><author>Merz, David C ; Alves, Georges ; Kawano, Takehiro ; Zheng, Hong ; Culotti, Joseph G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-b3adc4922b0587049c09c751094edfa9906b4e0c0ea666fa11618c46613c161e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>C. elegans</topic><topic>Caenorhabditis elegans - cytology</topic><topic>Caenorhabditis elegans - genetics</topic><topic>Caenorhabditis elegans - growth & development</topic><topic>Caenorhabditis elegans - metabolism</topic><topic>Caenorhabditis elegans Proteins - genetics</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Cell migrations</topic><topic>Cell Movement - genetics</topic><topic>Disorders of Sex Development</topic><topic>Female</topic><topic>Genes, Helminth</topic><topic>Gonads - cytology</topic><topic>Gonads - growth & development</topic><topic>Gonads - metabolism</topic><topic>Growth Substances - genetics</topic><topic>Growth Substances - metabolism</topic><topic>Helminth Proteins - genetics</topic><topic>Helminth Proteins - metabolism</topic><topic>Larva - cytology</topic><topic>Larva - growth & development</topic><topic>Larva - metabolism</topic><topic>Male</topic><topic>Membrane Proteins</topic><topic>Muscles - metabolism</topic><topic>Mutation</topic><topic>Nerve Tissue Proteins</topic><topic>Netrins</topic><topic>Organogenesis</topic><topic>Perlecan</topic><topic>Phenotype</topic><topic>Protein Tyrosine Phosphatases - genetics</topic><topic>Proteoglycans - genetics</topic><topic>Proteoglycans - metabolism</topic><topic>Receptor-Like Protein Tyrosine Phosphatases</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Fibroblast Growth Factor - genetics</topic><topic>Signal Transduction</topic><topic>UNC-52</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Merz, David C</creatorcontrib><creatorcontrib>Alves, Georges</creatorcontrib><creatorcontrib>Kawano, Takehiro</creatorcontrib><creatorcontrib>Zheng, Hong</creatorcontrib><creatorcontrib>Culotti, Joseph G</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Merz, David C</au><au>Alves, Georges</au><au>Kawano, Takehiro</au><au>Zheng, Hong</au><au>Culotti, Joseph G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>UNC-52/Perlecan affects gonadal leader cell migrations in c. elegans hermaphrodites through alterations in growth factor signaling</atitle><jtitle>Developmental biology</jtitle><addtitle>Dev Biol</addtitle><date>2003-04-01</date><risdate>2003</risdate><volume>256</volume><issue>1</issue><spage>174</spage><epage>187</epage><pages>174-187</pages><issn>0012-1606</issn><eissn>1095-564X</eissn><abstract>The
unc-52 gene of
Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These
unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of
unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecules, including EGL-17/FGF, UNC-129/TGF-β, DBL-1/TGF-β, and EGL-20/WNT. We propose that UNC-52 serves dual roles in
C. elegans larval development in the maintenance of muscle structure and the regulation of growth factor-like signaling pathways.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12654300</pmid><doi>10.1016/S0012-1606(03)00014-9</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-5548-0270</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Developmental biology, 2003-04, Vol.256 (1), p.174-187 |
| issn | 0012-1606 1095-564X |
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| subjects | Animals Animals, Genetically Modified C. elegans Caenorhabditis elegans - cytology Caenorhabditis elegans - genetics Caenorhabditis elegans - growth & development Caenorhabditis elegans - metabolism Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Cell migrations Cell Movement - genetics Disorders of Sex Development Female Genes, Helminth Gonads - cytology Gonads - growth & development Gonads - metabolism Growth Substances - genetics Growth Substances - metabolism Helminth Proteins - genetics Helminth Proteins - metabolism Larva - cytology Larva - growth & development Larva - metabolism Male Membrane Proteins Muscles - metabolism Mutation Nerve Tissue Proteins Netrins Organogenesis Perlecan Phenotype Protein Tyrosine Phosphatases - genetics Proteoglycans - genetics Proteoglycans - metabolism Receptor-Like Protein Tyrosine Phosphatases Receptors, Cell Surface - genetics Receptors, Fibroblast Growth Factor - genetics Signal Transduction UNC-52 |
| title | UNC-52/Perlecan affects gonadal leader cell migrations in c. elegans hermaphrodites through alterations in growth factor signaling |
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