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NorpA and itpr mutants reveal roles for phospholipase C and inositol (1,4,5)- trisphosphate receptor in Drosophila melanogaster renal function.
J Exp Biol. 2003 Mar; 206(Pt 5):901-11.JE

Abstract

Mutants of norpA, encoding phospholipase C beta (PLC beta), and itpr, encoding inositol (1,4,5)-trisphosphate receptor (IP(3)R), both attenuate response to diuretic peptides of Drosophila melanogaster renal (Malpighian) tubules. Intact tubules from norpA mutants severely reduced diuresis stimulated by the principal cell- and stellate cell-specific neuropeptides, CAP(2b) and Drosophila leucokinin (Drosokinin), respectively, suggesting a role for PLC beta in both these cell types. Measurement of IP(3) production in wild-type tubules and in Drosokinin-receptor-transfected S2 cells stimulated with CAP(2b) and Drosokinin, respectively, confirmed that both neuropeptides elevate IP(3) levels. In itpr hypomorphs, basal IP(3) levels are lower, although CAP(2b)-stimulated IP(3) levels are not significantly reduced compared with wild type. However, CAP(2b)-stimulated fluid transport is significantly reduced in itpr alleles. Rescue of the itpr(90B.0) allele with wild-type itpr restores CAP(2b)-stimulated fluid transport levels to wild type. Drosokinin-stimulated fluid transport is also reduced in homozygous and heteroallelic itpr mutants. Measurements of cytosolic calcium levels in intact tubules of wild-type and itpr mutants using targeted expression of the calcium reporter, aequorin, show that mutations in itpr attenuated both CAP(2b)- and Drosokinin-stimulated calcium responses. The reductions in calcium signals are associated with corresponding reductions in fluid transport rates. Thus, we describe a role for norpA and itpr in renal epithelia and show that both CAP(2b) and Drosokinin are PLC beta-dependent, IP(3)-mobilising neuropeptides in Drosophila. IP(3)R contributes to the calcium signalling cascades initiated by these peptides in both principal and stellate cells.

Authors+Show Affiliations

Institute of Biomedical and Life Sciences, Division of Molecular Genetics, University of Glasgow, Glasgow G11 6NU, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12547945

Citation

Pollock, Valerie P., et al. "NorpA and Itpr Mutants Reveal Roles for Phospholipase C and Inositol (1,4,5)- Trisphosphate Receptor in Drosophila Melanogaster Renal Function." The Journal of Experimental Biology, vol. 206, no. Pt 5, 2003, pp. 901-11.
Pollock VP, Radford JC, Pyne S, et al. NorpA and itpr mutants reveal roles for phospholipase C and inositol (1,4,5)- trisphosphate receptor in Drosophila melanogaster renal function. J Exp Biol. 2003;206(Pt 5):901-11.
Pollock, V. P., Radford, J. C., Pyne, S., Hasan, G., Dow, J. A., & Davies, S. A. (2003). NorpA and itpr mutants reveal roles for phospholipase C and inositol (1,4,5)- trisphosphate receptor in Drosophila melanogaster renal function. The Journal of Experimental Biology, 206(Pt 5), 901-11.
Pollock VP, et al. NorpA and Itpr Mutants Reveal Roles for Phospholipase C and Inositol (1,4,5)- Trisphosphate Receptor in Drosophila Melanogaster Renal Function. J Exp Biol. 2003;206(Pt 5):901-11. PubMed PMID: 12547945.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NorpA and itpr mutants reveal roles for phospholipase C and inositol (1,4,5)- trisphosphate receptor in Drosophila melanogaster renal function. AU - Pollock,Valerie P, AU - Radford,Jonathan C, AU - Pyne,Susan, AU - Hasan,Gaiti, AU - Dow,Julian A T, AU - Davies,Shireen-A, PY - 2003/1/28/pubmed PY - 2003/9/17/medline PY - 2003/1/28/entrez SP - 901 EP - 11 JF - The Journal of experimental biology JO - J Exp Biol VL - 206 IS - Pt 5 N2 - Mutants of norpA, encoding phospholipase C beta (PLC beta), and itpr, encoding inositol (1,4,5)-trisphosphate receptor (IP(3)R), both attenuate response to diuretic peptides of Drosophila melanogaster renal (Malpighian) tubules. Intact tubules from norpA mutants severely reduced diuresis stimulated by the principal cell- and stellate cell-specific neuropeptides, CAP(2b) and Drosophila leucokinin (Drosokinin), respectively, suggesting a role for PLC beta in both these cell types. Measurement of IP(3) production in wild-type tubules and in Drosokinin-receptor-transfected S2 cells stimulated with CAP(2b) and Drosokinin, respectively, confirmed that both neuropeptides elevate IP(3) levels. In itpr hypomorphs, basal IP(3) levels are lower, although CAP(2b)-stimulated IP(3) levels are not significantly reduced compared with wild type. However, CAP(2b)-stimulated fluid transport is significantly reduced in itpr alleles. Rescue of the itpr(90B.0) allele with wild-type itpr restores CAP(2b)-stimulated fluid transport levels to wild type. Drosokinin-stimulated fluid transport is also reduced in homozygous and heteroallelic itpr mutants. Measurements of cytosolic calcium levels in intact tubules of wild-type and itpr mutants using targeted expression of the calcium reporter, aequorin, show that mutations in itpr attenuated both CAP(2b)- and Drosokinin-stimulated calcium responses. The reductions in calcium signals are associated with corresponding reductions in fluid transport rates. Thus, we describe a role for norpA and itpr in renal epithelia and show that both CAP(2b) and Drosokinin are PLC beta-dependent, IP(3)-mobilising neuropeptides in Drosophila. IP(3)R contributes to the calcium signalling cascades initiated by these peptides in both principal and stellate cells. SN - 0022-0949 UR - https://www.unboundmedicine.com/medline/citation/12547945/NorpA_and_itpr_mutants_reveal_roles_for_phospholipase_C_and_inositol__145___trisphosphate_receptor_in_Drosophila_melanogaster_renal_function_ L2 - http://jeb.biologists.org/cgi/pmidlookup?view=long&pmid=12547945 DB - PRIME DP - Unbound Medicine ER -