Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-1-26
pubmed:abstractText
The Lyra mutation was first described by Jerry Coyne in 1935. Lyra causes recessive pupal lethality and adult heterozygous Lyra mutants exhibit a dominant loss of the anterior and posterior wing margins. Unlike many mutations that cause loss of wing tissue (e.g., scalloped, Beadex, cut, and apterous-Xasta), Lyra wing discs do not exhibit increased necrotic or apoptotic cell death, nor do they show altered BrdU incorporation. However, during wing disc eversion, loss of the anterior and posterior wing margins is apparent. We have previously shown that senseless, a gene that is necessary and sufficient for peripheral nervous system (PNS) development, is allelic to Lyra. Here we show by several genetic criteria that Lyra alleles are neomorphic alleles of senseless that cause ectopic expression of SENSELESS in the wing pouch. Similarly, overexpression of SENSELESS in the wing disc causes loss of wing margin tissue, thereby mimicking the Lyra phenotype. Lyra mutants display aberrant expression of DELTA, VESTIGIAL, WINGLESS, and CUT. As in Lyra mutants, overexpression of SENSELESS in some areas of the wing pouch also leads to loss of WINGLESS and CUT. In summary, our data indicate that overexpression of SENSELESS causes a severe reduction in NOTCH signaling that in turn may lead to decreased transcription of several key genes required for wing development, leading to a failure in cell proliferation and loss of wing margin tissue.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-10221902, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-10471706, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-10975525, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-1349545, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-1353736, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-2044964, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-2558050, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-3117374, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-3119404, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-4624779, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-4979601, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-5692588, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-7555709, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-7671307, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-7720583, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8060613, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8125190, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8127364, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8162860, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8330519, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8330528, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8575321, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8600026, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8700202, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8749396, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8851804, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8951063, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-8970725, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-9043068, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-9409832, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-9570768, http://linkedlifedata.com/resource/pubmed/commentcorrection/11139511-9665132
pubmed:keyword
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0016-6731
pubmed:author
pubmed:issnType
Print
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
307-15
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Drosophila Lyra mutations are gain-of-function mutations of senseless.
pubmed:affiliation
Howard Hughes Medical Institute, Program in Developmental Biology, Division of Neuroscience, Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't