Reference Report

Reference
Citation	Rhea, J.M., Wegener, C., Bender, M. (2010). The proprotein convertase encoded by amontillado (amon) is required in Drosophila corpora cardiaca endocrine cells producing the glucose regulatory hormone AKH. PLoS Genet. 6(5): e1000967. (Export to RIS)
FlyBase ID	FBrf0210955
Publication Type	Research paper
PubMed ID	20523747
PubMed Abstract	Peptide hormones are potent signaling molecules that coordinate animal physiology, behavior, and development. A key step in activation of these peptide signals is their proteolytic processing from propeptide precursors by a family of proteases, the subtilisin-like proprotein convertases (PCs). Here, we report the functional dissection of amontillado (amon), which encodes the Drosophila homolog of the mammalian PC2 protein, using cell-type specific inactivation and rescue experiments, and we show that amon is required in the islet-like adipokinetic hormone (AKH)-producing cells that regulate sugar homeostasis. In Drosophila, AKH acts analogously to vertebrate glucagon to increase circulating sugar levels from energy stores, while insulin-like peptides (DILPs) act to decrease sugar levels. amon mutant larvae have significantly reduced hemolymph sugar levels, and thus phenocopy larvae where the AKH-producing cells in the corpora cardiaca have been ablated. Reduction of amon expression in these cells via cell-specific RNA inactivation also results in larvae with reduced sugar levels while expression of amon in AKH cells in an amon mutant background rescues hypoglycemia. Hypoglycemia in larvae resulting from amon RNA inactivation in the AKH cells can be rescued by global expression of the akh gene. Finally, mass spectrometric profiling shows that the production of mature AKH is inhibited in amon mutants. Our data indicate that amon function in the AKH cells is necessary to maintain normal sugar homeostasis, that amon functions upstream of akh, and that loss of mature AKH is correlated with loss of amon activity. These observations indicate that the AKH propeptide is a proteolytic target of the amon proprotein convertase and provide evidence for a conserved role of PC2 in processing metabolic peptide hormones.
DOI	10.1371/journal.pgen.1000967
Related Publication(s)
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
Language of Publication	English
Additional Languages of Abstract
Also Published As
Parent Publication
Publication Type	Journal
Abbreviation	PLoS Genet.
Title	PLoS Genetics
Publication Year	2005-
ISBN/ISSN	1553-7404 1553-7390
Data from Reference
Aberrations (1)
	Df(3R)Tl-X
Alleles (11)
	Akh^hs.PK amon^C241Y amon^{dsRNA.Scer\UAS.cBa} amon^hs.PS amon^Q178st amon^Scer\UAS.cRa Scer\GAL4^Act.PU Scer\GAL4^Akh.PL Scer\GAL4^amon.PR Scer\GAL4^hs.PU w^+mC
Constructs (8)
	P{Act-GAL4.U} P{Akh-gal4.L} P{amon-GAL4.R} P{hs-Akh.K} P{hs-amon.S} P{hs-GAL4.U} P{UAS-amon.R} P{UAS-amon-RNAi}
Genes (4)
	Akh amon Scer\GAL4 w
Insertions (3)
	P{amon-GAL4.R}91D P{UAS-amon.R}40L P{UAS-amon-RNAi}28b
Transcripts (1)
	Scer\GAL4^amon.PRRA