Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-2-21
pubmed:abstractText
Rapid larval growth is essential in the development of most metazoans. In this article, we show that bene, a gene previously identified on the basis of its oogenesis defects, is also required for larval growth and viability. We show that all bene alleles disrupt gatA, which encodes the Drosophila homolog of glutamyl-tRNA(Gln) amidotransferase subunit A (GatA). bene alleles are now referred to as gatA. GatA proteins are highly conserved throughout eukaryotes and many prokaryotes. These enzymes are required for proper translation of the proteins encoded by the mitochondrial genome and by many eubacterial genomes. Mitotic and endoreplicating tissues in Drosophila gatA loss-of-function mutants grow slowly and never achieve wild-type size, and gatA larvae die before pupariation. gatA mutant eye clones exhibit growth and differentiation defects, indicating that gatA expression is required cell autonomously for normal growth. The gatA gene is widely expressed in mitotic and endoreplicating tissues.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-10225996, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-10679387, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-10858562, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-11054409, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-11348589, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-11517449, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-11832249, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-12642658, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-12824352, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-12930750, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-14641047, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-14651932, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-15238527, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-15574749, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-15611111, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-15692573, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-15838513, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-15998720, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-16326395, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-16381917, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-16421301, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-17115029, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-17139322, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-17435247, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-17622252, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-2231712, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-3117373, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-3921555, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-8307009, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-9287027, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-9342308, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-9342321, http://linkedlifedata.com/resource/pubmed/commentcorrection/18245325-9677706
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0016-6731
pubmed:author
pubmed:issnType
Print
pubmed:volume
178
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
979-87
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Mutations in the Drosophila mitochondrial tRNA amidotransferase, bene/gatA, cause growth defects in mitotic and endoreplicating tissues.
pubmed:affiliation
Department of Natural Sciences, Fordham University, New York, New York 10023, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural