A histological and ultrastructural analysis of developmental defects produced by the mutation, lethal(1)myospheroid, in Drosophila melanogaster
The recessive embryonic lethal, lethal(1)myospheroid, is located at 21.7 map units on the X chromosome in Drosophila melanogaster. Embryos hemizygous for this mutation appear to develop normally until the time of the first muscular contractions. Due to the physical stress of these initial contractio...
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Veröffentlicht in: | Developmental biology 1981-01, Vol.86 (2), p.393-402 |
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description | The recessive embryonic lethal,
lethal(1)myospheroid, is located at 21.7 map units on the X chromosome in
Drosophila melanogaster. Embryos hemizygous for this mutation appear to develop normally until the time of the first muscular contractions. Due to the physical stress of these initial contractions, dramatic tissue separations occur, which characterize the phenotype of this mutation. The dorsal suture separates with the herniation of midgut and nervous tissue, and the somatic and visceral muscles retract from their sites of attachment. An ultrastructural examination of the development of the muscle attachment sites in these embryos indicates that in
1(1)mys embryos there is a delay in the formation of normal cell-cell attachments. At the muscle-tendon cell junction, the deposition of the apparently normal extracellular matrix of this desmosomal attachment occurs considerably later in development than normal. The
1(1)mys locus apparently makes a product which is either defective, made more slowly, or produced in smaller amounts than normal. The
1(1)mys product is probably necessary for the production of a component of the extracellular matrix of cell-cell attachments. |
doi_str_mv | 10.1016/0012-1606(81)90197-4 |
format | Article |
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lethal(1)myospheroid, is located at 21.7 map units on the X chromosome in
Drosophila melanogaster. Embryos hemizygous for this mutation appear to develop normally until the time of the first muscular contractions. Due to the physical stress of these initial contractions, dramatic tissue separations occur, which characterize the phenotype of this mutation. The dorsal suture separates with the herniation of midgut and nervous tissue, and the somatic and visceral muscles retract from their sites of attachment. An ultrastructural examination of the development of the muscle attachment sites in these embryos indicates that in
1(1)mys embryos there is a delay in the formation of normal cell-cell attachments. At the muscle-tendon cell junction, the deposition of the apparently normal extracellular matrix of this desmosomal attachment occurs considerably later in development than normal. The
1(1)mys locus apparently makes a product which is either defective, made more slowly, or produced in smaller amounts than normal. The
1(1)mys product is probably necessary for the production of a component of the extracellular matrix of cell-cell attachments.</description><identifier>ISSN: 0012-1606</identifier><identifier>EISSN: 1095-564X</identifier><identifier>DOI: 10.1016/0012-1606(81)90197-4</identifier><identifier>PMID: 6793430</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>animal anatomy ; animal morphology ; Animals ; arthropods ; Drosophila melanogaster - cytology ; Drosophila melanogaster - genetics ; Drosophila melanogaster - ultrastructure ; Embryo, Nonmammalian - ultrastructure ; entomology ; Female ; Genes, Lethal ; Microscopy, Electron ; Muscles - cytology ; Muscles - embryology ; Mutation ; X Chromosome</subject><ispartof>Developmental biology, 1981-01, Vol.86 (2), p.393-402</ispartof><rights>1981</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-92c0020645ec78eb98263653e7bd888f4ef51048071062b26318d0c5f71ddff83</citedby><cites>FETCH-LOGICAL-c381t-92c0020645ec78eb98263653e7bd888f4ef51048071062b26318d0c5f71ddff83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0012-1606(81)90197-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6793430$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Newman, Samuel M.</creatorcontrib><creatorcontrib>Wright, Theodore R.F.</creatorcontrib><title>A histological and ultrastructural analysis of developmental defects produced by the mutation, lethal(1)myospheroid, in Drosophila melanogaster</title><title>Developmental biology</title><addtitle>Dev Biol</addtitle><description>The recessive embryonic lethal,
lethal(1)myospheroid, is located at 21.7 map units on the X chromosome in
Drosophila melanogaster. Embryos hemizygous for this mutation appear to develop normally until the time of the first muscular contractions. Due to the physical stress of these initial contractions, dramatic tissue separations occur, which characterize the phenotype of this mutation. The dorsal suture separates with the herniation of midgut and nervous tissue, and the somatic and visceral muscles retract from their sites of attachment. An ultrastructural examination of the development of the muscle attachment sites in these embryos indicates that in
1(1)mys embryos there is a delay in the formation of normal cell-cell attachments. At the muscle-tendon cell junction, the deposition of the apparently normal extracellular matrix of this desmosomal attachment occurs considerably later in development than normal. The
1(1)mys locus apparently makes a product which is either defective, made more slowly, or produced in smaller amounts than normal. The
1(1)mys product is probably necessary for the production of a component of the extracellular matrix of cell-cell attachments.</description><subject>animal anatomy</subject><subject>animal morphology</subject><subject>Animals</subject><subject>arthropods</subject><subject>Drosophila melanogaster - cytology</subject><subject>Drosophila melanogaster - genetics</subject><subject>Drosophila melanogaster - ultrastructure</subject><subject>Embryo, Nonmammalian - ultrastructure</subject><subject>entomology</subject><subject>Female</subject><subject>Genes, Lethal</subject><subject>Microscopy, Electron</subject><subject>Muscles - cytology</subject><subject>Muscles - embryology</subject><subject>Mutation</subject><subject>X Chromosome</subject><issn>0012-1606</issn><issn>1095-564X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1981</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kd1q3DAQhUVpSbdp36CluioJxK1k2bJ8UwhJ-gOBXrSB3glZGq1VZMuR5MA-RV-52uySy4JgQOfMzOEbhN5S8pESyj8RQuuKcsLPBD3vCe27qnmGNpT0bdXy5vdztHmyvESvUvpDCGFCsBN0wrueNYxs0N9LPLqUgw9bp5XHajZ49TmqlOOq8xof_5TfJZdwsNjAA_iwTDDnohiwoHPCSwxm1WDwsMN5BDytWWUX5gvsIY_Kn9HzaRfSMkIMzlxgN-PrGFJYRucVnsCrOWzLSoiv0QurfII3x3qK7r7c_Lr6Vt3--Pr96vK20kzQXPW1JqQmvGlBdwKGXtSc8ZZBNxghhG3AtpQ0gnSU8HooIhWG6NZ21BhrBTtFHw5zS_T7FVKWk0safEkCYU2yY7xjBV8xNgejLoFTBCuX6CYVd5ISub-D3EOWe8hSUPl4B9mUtnfH-eswgXlqOoIv-vuDblWQahtdknc_67KvvLotE4vj88EBBcODgyiTdjAXyi4W6NIE9_8I_wCeAaKc</recordid><startdate>19810101</startdate><enddate>19810101</enddate><creator>Newman, Samuel M.</creator><creator>Wright, Theodore R.F.</creator><general>Elsevier Inc</general><scope>FBQ</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>7X8</scope></search><sort><creationdate>19810101</creationdate><title>A histological and ultrastructural analysis of developmental defects produced by the mutation, lethal(1)myospheroid, in Drosophila melanogaster</title><author>Newman, Samuel M. ; Wright, Theodore R.F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-92c0020645ec78eb98263653e7bd888f4ef51048071062b26318d0c5f71ddff83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1981</creationdate><topic>animal anatomy</topic><topic>animal morphology</topic><topic>Animals</topic><topic>arthropods</topic><topic>Drosophila melanogaster - cytology</topic><topic>Drosophila melanogaster - genetics</topic><topic>Drosophila melanogaster - ultrastructure</topic><topic>Embryo, Nonmammalian - ultrastructure</topic><topic>entomology</topic><topic>Female</topic><topic>Genes, Lethal</topic><topic>Microscopy, Electron</topic><topic>Muscles - cytology</topic><topic>Muscles - embryology</topic><topic>Mutation</topic><topic>X Chromosome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Newman, Samuel M.</creatorcontrib><creatorcontrib>Wright, Theodore R.F.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Newman, Samuel M.</au><au>Wright, Theodore R.F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A histological and ultrastructural analysis of developmental defects produced by the mutation, lethal(1)myospheroid, in Drosophila melanogaster</atitle><jtitle>Developmental biology</jtitle><addtitle>Dev Biol</addtitle><date>1981-01-01</date><risdate>1981</risdate><volume>86</volume><issue>2</issue><spage>393</spage><epage>402</epage><pages>393-402</pages><issn>0012-1606</issn><eissn>1095-564X</eissn><abstract>The recessive embryonic lethal,
lethal(1)myospheroid, is located at 21.7 map units on the X chromosome in
Drosophila melanogaster. Embryos hemizygous for this mutation appear to develop normally until the time of the first muscular contractions. Due to the physical stress of these initial contractions, dramatic tissue separations occur, which characterize the phenotype of this mutation. The dorsal suture separates with the herniation of midgut and nervous tissue, and the somatic and visceral muscles retract from their sites of attachment. An ultrastructural examination of the development of the muscle attachment sites in these embryos indicates that in
1(1)mys embryos there is a delay in the formation of normal cell-cell attachments. At the muscle-tendon cell junction, the deposition of the apparently normal extracellular matrix of this desmosomal attachment occurs considerably later in development than normal. The
1(1)mys locus apparently makes a product which is either defective, made more slowly, or produced in smaller amounts than normal. The
1(1)mys product is probably necessary for the production of a component of the extracellular matrix of cell-cell attachments.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>6793430</pmid><doi>10.1016/0012-1606(81)90197-4</doi><tpages>10</tpages></addata></record> |
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subjects | animal anatomy animal morphology Animals arthropods Drosophila melanogaster - cytology Drosophila melanogaster - genetics Drosophila melanogaster - ultrastructure Embryo, Nonmammalian - ultrastructure entomology Female Genes, Lethal Microscopy, Electron Muscles - cytology Muscles - embryology Mutation X Chromosome |
title | A histological and ultrastructural analysis of developmental defects produced by the mutation, lethal(1)myospheroid, in Drosophila melanogaster |
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