A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Dolezal, T., Dolezelova, E., Zurovec, M., Bryant, P.J. (2005). A role for adenosine deaminase in Drosophila larval development.  PLoS Biol. 3(7): e201. (Export to RIS)
FlyBase ID FBrf0188209
Publication Type Research paper
PubMed ID 15907156
PubMed Abstract Adenosine deaminase (ADA) is an enzyme present in all organisms that catalyzes the irreversible deamination of adenosine and deoxyadenosine to inosine and deoxyinosine. Both adenosine and deoxyadenosine are biologically active purines that can have a deep impact on cellular physiology; notably, ADA deficiency in humans causes severe combined immunodeficiency. We have established a Drosophila model to study the effects of altered adenosine levels in vivo by genetic elimination of adenosine deaminase-related growth factor-A (ADGF-A), which has ADA activity and is expressed in the gut and hematopoietic organ. Here we show that the hemocytes (blood cells) are the main regulator of adenosine in the Drosophila larva, as was speculated previously for mammals. The elevated level of adenosine in the hemolymph due to lack of ADGF-A leads to apparently inconsistent phenotypic effects: precocious metamorphic changes including differentiation of macrophage-like cells and fat body disintegration on one hand, and delay of development with block of pupariation on the other. The block of pupariation appears to involve signaling through the adenosine receptor (AdoR), but fat body disintegration, which is promoted by action of the hemocytes, seems to be independent of the AdoR. The existence of such an independent mechanism has also been suggested in mammals.
DOI 10.1371/journal.pbio.0030201
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Language of Publication English
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Publication Type Journal
Abbreviation PLoS Biol.
Title PLoS Biology
Publication Year 2003-
ISBN/ISSN 1545-7885 1544-9173
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