Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2000-11-9
pubmed:abstractText
semang (sag), a mutation isolated as a suppressor of Drosophila Src42A, has previously been shown to affect some receptor tyrosine kinase mediated embryonic processes. Here we show that sag specifically affects the development of R1, R6 and R7 photoreceptor cells in a cell-autonomous manner. These cells are absent in the mutant at the time when they normally appear in the ommatidial pre-clusters. Genetic analyses suggest that sag functions downstream of, or parallel to, Mapk and Yan in the photoreceptor differentiation pathway. The autonomous requirement of sag for R1/R6/R7 development could be explained by a selective impairment of the late, but not early, rounds of Egfr-induced precursor cell assembly by the sag mutations. Egfr signaling is highly regulated by autocrine or paracrine mechanisms in different cells. Knowing that the photoreceptor cluster formation is a complex process involving dynamic changes in cell-cell contact, our hypothesis is that the sag alleles affected certain special aspects of Egfr-signaling that are unique for the recruitment of R1/R6/R7 cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0925-4773
pubmed:author
pubmed:issnType
Print
pubmed:volume
95
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-22
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
semang affects the development of a subset of cells in the Drosophila compound eye.
pubmed:affiliation
Department of Molecular Biosciences, The University of Kansas, Lawrence, KS 66045, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't