Reference Report

Reference
Citation	Hewes, R.S., Gu, T., Brewster, J.A., Qu, C., Zhao, T. (2006). Regulation of secretory protein expression in mature cells by DIMM, a basic helix-loop-helix neuroendocrine differentiation factor. J. Neurosci. 26(30): 7860--7869. (Export to RIS)
FlyBase ID	FBrf0192298
Publication Type	Research paper
PubMed ID	16870731
PubMed Abstract	During differentiation, neuroendocrine cells acquire highly amplified capacities to synthesize neuropeptides to overcome dilution of these signals in the general circulation. Once mature, the normal functioning of integrated physiological systems requires that neuroendocrine cells remain plastic to dramatically alter neuropeptide expression for long periods in response to hormonal and electrical cues. The mechanisms underlying the long-term regulation of neuroendocrine systems are poorly understood. Here we show that the Drosophila basic helix-loop-helix protein DIMM, a critical regulator of neuroendocrine cell differentiation, controls secretory capacity in mature neurons. DIMM expression began embryonically but persisted in adults. Through spatial and temporal manipulation of transgene expression in vivo, we defined two phases of prosecretory DIMM activity. During an embryonic critical window, DIMM controlled the differentiation of amplified expression of the neuropeptide leucokinin. At the onset of metamorphosis, levels of DIMM decreased in the insulin-producing cells (IPCs) in parallel with a marked reduction in levels of Drosophila insulin-like peptide 2 and a key neuropeptide biosynthetic enzyme peptidylglycine alpha-monooxygenase (PHM). Overexpression of DIMM in the IPCs prevented the decrease in PHM levels at this stage. In addition, transient overexpression of DIMM in adults produced a dramatic increase in PHM levels in numerous neurons located throughout the brain. These findings provide insights into the mechanisms controlling the maintenance of differentiated cell states, and they suggest an effective means for dynamically adjusting the strength of hormonal signals in diverse homeostatic systems.
DOI	10.1523/JNEUROSCI.1759-06.2006
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Language of Publication	English
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Publication Type	Journal
Abbreviation	J. Neurosci.
Title	Journal of Neuroscience
Publication Year	1981-
ISBN/ISSN	0270-6474 1529-2401
Data from Reference
Aberrations (1)
	Df(2L)Rev4
Alleles (9)
	Avic\GFP^Scer\UAS.cYa dimm⁹²⁹ dimm^Rev8 dimm^{Scer\UAS.T:Hsap\MYC} Mmus\Cd8a^{Scer\UAS.T:Avic\GFP} Scer\GAL4^ap-md544 Scer\GAL4^dimm-929 Scer\GAL4^Ilp2.PR Scer\GAL80^ts.αTub84B
Constructs (5)
	P{Ilp2-GAL4.R} P{tubP-GAL80^ts} P{UAS-dimm.MYC} P{UAS-GFP.Y} P{UAS-mCD8::GFP.L}
Genes (8)
	Avic\GFP dimm Ilp2 Lk Mmus\Cd8a Phm Scer\GAL4 Scer\GAL80
Insertions (7)
	P{GawB}ap^md544 P{GawB}dimm⁹²⁹ P{tubP-GAL80^ts}7 P{tubP-GAL80^ts}20 P{UAS-dimm.MYC}2-A-3 P{UAS-GFP.Y}B1 P{UAS-mCD8::GFP.L}LL5
Transcripts (1)
	Scer\GAL4^dimm-929RA