scholarly journals Effects of gap junction misexpression on synapses between auditory sensory neurons and the giant fiber of Drosophila melanogaster

2018 ◽  
Author(s):  
Sami H. Jezzini ◽  
Amelia Merced ◽  
Jonathan M. Blagburn
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Gap Junctions ◽  
Sensory Neurons ◽  
De Novo ◽  
Dye Coupling ◽  
Giant Fiber ◽  
Mixed Synapses ◽  
Chemical Synapses ◽  
Gap Junctional

AbstractThe synapse between auditory Johnston’s Organ neurons (JONs) and the giant fiber (GF) of Drosophila is structurally mixed, being composed of cholinergic chemical synapses and Neurobiotin-(NB) permeable gap junctions, which consist of the innexin Shaking-B (ShakB). Misexpression of one ShakB isoform, ShakB(N+16), in a subset of JONs that do not normally form gap junctions, results in their de novo dye coupling to the GF. This is similar to the effect of misexpression of the transcription factor Engrailed (En) in these same neurons, which also causes the formation of additional chemical synapses. In order to test the hypothesis that ShakB misexpression would similarly affect the distribution of chemical synapses, fluorescently-labeled presynaptic active zone protein (Brp) was expressed in JONs and the changes in its distribution were assayed with confocal microscopy. Both ShakB(N+16) and En increased the dye-coupling of JONs with the GF, indicating the formation of ectopic gap junctions. Conversely, expression of the ‘incorrect’ isoform, ShakB(N) abolishes dye coupling. However, while En misexpression increased the chemical contacts with the GF and the amount of GF medial branching, ShakB misexpression did not. ShakB immunocytochemistry showed that misexpression of ShakB(N+16) increases gap junctional plaques in JON axons but ShakB(N) does not. We conclude that both subsets of JON form chemical synapses onto the GF dendrites but only one population forms gap junctions, comprised of ShakB(N+16). Misexpression of this isoform in all JONs does not result in the formation of new mixed synapses but in the insertion of gap junctions, presumably at the sites of existing chemical synaptic contacts with the GF.

scholarly journals Shaking B Mediates Synaptic Coupling between Auditory Sensory Neurons and the Giant Fiber of Drosophila melanogaster

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0152211 ◽  
Author(s):  
Adeline P. Pézier ◽  
Sami H. Jezzini ◽  
Jonathan P. Bacon ◽  
Jonathan M. Blagburn
Keyword(s):  
Drosophila Melanogaster ◽  
Sensory Neurons ◽  
Synaptic Coupling ◽  
Giant Fiber

In vivo modulation of gap junctions and dye coupling between B-cells of the intact pancreatic islet

Diabetes ◽  
1983 ◽  
Vol 32 (9) ◽  
pp. 858-868 ◽  
Author(s):  
P. Meda ◽  
R. L. Michaels ◽  
P. A. Halban ◽  
L. Orci ◽  
J. D. Sheridan
Keyword(s):  
B Cells ◽  
Gap Junctions ◽  
Pancreatic Islet ◽  
Dye Coupling

scholarly journals A closed-loop optogenetic screen for neurons controlling feeding in Drosophila

2021 ◽  
Author(s):  
Celia K S Lau ◽  
Meghan Jelen ◽  
Michael D Gordon
Keyword(s):  
Drosophila Melanogaster ◽  
Expression Pattern ◽  
Sensory Neurons ◽  
Closed Loop ◽  
Higher Order ◽  
Taste Detection ◽  
Proof Of Principle ◽  
Feeding Circuits

Abstract Feeding is an essential part of animal life that is greatly impacted by the sense of taste. Although the characterization of taste-detection at the periphery has been extensive, higher order taste and feeding circuits are still being elucidated. Here, we use an automated closed-loop optogenetic activation screen to detect novel taste and feeding neurons in Drosophila melanogaster. Out of 122 Janelia FlyLight Project GAL4 lines preselected based on expression pattern, we identify six lines that acutely promote feeding and 35 lines that inhibit it. As proof of principle, we follow up on R70C07-GAL4, which labels neurons that strongly inhibit feeding. Using split-GAL4 lines to isolate subsets of the R70C07-GAL4 population, we find both appetitive and aversive neurons. Furthermore, we show that R70C07-GAL4 labels putative second-order taste interneurons that contact both sweet and bitter sensory neurons. These results serve as a resource for further functional dissection of fly feeding circuits.

Functions of transcription factor TRF2 Drosophila melanogaster

2008 ◽  
Vol 44 (3) ◽  
pp. 260-265
Author(s):  
D. V. Kopytova ◽  
M. R. Kopantseva ◽  
E. N. Nabirochkina ◽  
N. E. Vorobyova ◽  
S. G. Georgieva ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster

scholarly journals Drosophila Ana2 is a conserved centriole duplication factor

2010 ◽  
Vol 188 (3) ◽  
pp. 313-323 ◽  
Author(s):  
Naomi R. Stevens ◽  
Jeroen Dobbelaere ◽  
Kathrin Brunk ◽  
Anna Franz ◽  
Jordan W. Raff
Keyword(s):  
Drosophila Melanogaster ◽  
Caenorhabditis Elegans ◽  
De Novo ◽  
Protein Family ◽  
Centriole Duplication

In Caenorhabditis elegans, five proteins are required for centriole duplication: SPD-2, ZYG-1, SAS-5, SAS-6, and SAS-4. Functional orthologues of all but SAS-5 have been found in other species. In Drosophila melanogaster and humans, Sak/Plk4, DSas-6/hSas-6, and DSas-4/CPAP—orthologues of ZYG-1, SAS-6, and SAS-4, respectively—are required for centriole duplication. Strikingly, all three fly proteins can induce the de novo formation of centriole-like structures when overexpressed in unfertilized eggs. Here, we find that of eight candidate duplication factors identified in cultured fly cells, only two, Ana2 and Asterless (Asl), share this ability. Asl is now known to be essential for centriole duplication in flies, but no equivalent protein has been found in worms. We show that Ana2 is the likely functional orthologue of SAS-5 and that it is also related to the vertebrate STIL/SIL protein family that has been linked to microcephaly in humans. We propose that members of the SAS-5/Ana2/STIL family of proteins are key conserved components of the centriole duplication machinery.

scholarly journals Identification of target genes and a unique cis element regulated by IRF-8 in developing macrophages

Blood ◽  
2005 ◽  
Vol 106 (6) ◽  
pp. 1938-1947 ◽  
Author(s):  
Tomohiko Tamura ◽  
Pratima Thotakura ◽  
Tetsuya S. Tanaka ◽  
Minoru S. H. Ko ◽  
Keiko Ozato
Keyword(s):  
Transcription Factor ◽  
Cystatin C ◽  
Target Genes ◽  
De Novo ◽  
Consensus Sequence ◽  
Binding Motif ◽  
Microarray Gene Expression ◽  
Cathepsin C ◽  
Cis Element

Abstract Interferon regulatory factor-8 (IRF-8)/interferon consensus sequence–binding protein (ICSBP) is a transcription factor that controls myeloid-cell development. Microarray gene expression analysis of Irf-8-/- myeloid progenitor cells expressing an IRF-8/estrogen receptor chimera (which differentiate into macrophages after addition of estradiol) was used to identify 69 genes altered by IRF-8 during early differentiation (62 up-regulated and 7 down-regulated). Among them, 4 lysosomal/endosomal enzyme-related genes (cystatin C, cathepsin C, lysozyme, and prosaposin) did not require de novo protein synthesis for induction, suggesting that they were direct targets of IRF-8. We developed a reporter assay system employing a self-inactivating retrovirus and analyzed the cystatin C and cathepsin C promoters. We found that a unique cis element mediates IRF-8–induced activation of both promoters. Similar elements were also found in other IRF-8 target genes with a consensus sequence (GAAANN[N]GGAA) comprising a core IRF-binding motif and an Ets-binding motif; this sequence is similar but distinct from the previously reported Ets/IRF composite element. Chromatin immunoprecipitation assays demonstrated that IRF-8 and the PU.1 Ets transcription factor bind to this element in vivo. Collectively, these data indicate that IRF-8 stimulates transcription of target genes through a novel cis element to specify macrophage differentiation.

scholarly journals Low pH enhances connexin32 degradation in the pancreatic acinar cell

2014 ◽  
Vol 307 (1) ◽  
pp. G24-G32 ◽  
Author(s):  
Anamika M. Reed ◽  
Thomas Kolodecik ◽  
Sohail Z. Husain ◽  
Fred S. Gorelick
Keyword(s):  
Gap Junctions ◽  
Acinar Cell ◽  
Intercellular Communication ◽  
Pancreatic Acinar Cell ◽  
Low Ph ◽  
Extracellular Ph ◽  
Gap Junctional Intercellular Communication ◽  
Junction Protein ◽  
Clinical Conditions ◽  
Gap Junctional

Decreased extracellular pH is observed in a number of clinical conditions and can sensitize to the development and worsen the severity of acute pancreatitis. Because intercellular communication through gap junctions is pH-sensitive and modulates pancreatitis responses, we evaluated the effects of low pH on gap junctions in the rat pancreatic acinar cell. Decreasing extracellular pH from 7.4 to 7.0 significantly inhibited gap junctional intracellular communication. Acidic pH also significantly reduced levels of connexin32, the predominant gap junction protein in acinar cells, and altered its localization. Increased degradation through the proteasomal, lysosomal, and autophagic pathways mediated the decrease in connexin32 under low-pH conditions. These findings provide the first evidence that low extracellular pH can regulate gap junctional intercellular communication by enhancing connexin degradation.

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