Molecular Basis of Amplification in Drosophila Phototransduction

Hardie, Roger C.; Martín, Fernando; Cochrane, Guy; Juusola, Mikko; Georgiev, Plamen; Raghu, Padinjat

doi:10.1016/s0896-6273(02)01048-6

Cited by 108 publications

(52 citation statements)

References 46 publications

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“…DAG, is blocked. This massive facilitation underscores other recent evidence indicating that DAG or a downstream metabolite is the essential messenger of excitation in Drosophila phototransduction (6,7,17).…”

Section: Discussionsupporting

confidence: 80%

“…This facilitation was effectively mimicked by the rdgA mutation encoding DAG kinase, suggesting that DGK normally suppresses bump amplitudes in norpA by metabolizing DAG (17). We performed similar experiments to see whether ATP depletion could also enhance sensitivity in norpA P24 .…”

Section: Spontaneous Currents and Light Responses In Norpamentioning

confidence: 90%

“…Consequently, on establishment of the whole-cell recording configuration there is an ongoing barrage of noisy inward current because of the summation of bumps with extremely long latencies generated by previous illumination. Depending on the severity of the allele, this activity decays in the dark during several seconds or minutes after which responses can be elicited from a quiet base line (15)(16)(17).…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

“…Less severe hypomorphic norpA mutants show reduced sensitivity with dramatically slowed kinetics (14 -16) and reduced amplification, as indicated by the small amplitude of responses to single photons known as quantum bumps (17). We recently discovered that sensitivity in norpA hypomorphs could be greatly facilitated by mutations in the retinal degeneration A (rdgA) gene and also by depletion of cytosolic ATP (17). This supports the hypothesis that DAG or its metabolites are excitatory messengers, because the rdgA gene encodes diacylglycerol kinase (DGK) (18), which is the major enzyme controlling DAG in most cells (19).…”

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confidence: 99%

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Rescue of Light Responses in the Drosophila “Null” Phospholipase C Mutant, norpA, by the Diacylglycerol Kinase Mutant, rdgA, and by Metabolic Inhibition

Hardie

Martín

Chyb³

et al. 2003

Journal of Biological Chemistry

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Light responses in Drosophila are reportedly abolished in severe mutants of the phospholipase C (PLC) gene, norpA. However, on establishing the whole-cell recording configuration in photoreceptors of the supposedly null allele, norpA P24 , we detected a small (ϳ15 pA) inward current that represented spontaneous light channel activity. The current decayed during ϳ20 min, after which tiny residual responses (<2 pA) were elicited by intense flashes. Both spontaneous currents and light responses appeared to be mediated by residual PLC activity, because they were enhanced by impairing diacylglycerol (DAG) kinase function by mutation (rdgA) or by restricting ATP but were reduced or abolished by a mutation of the PLC-specific G q ␣ subunit. It was reported recently that metabolic inhibition activated the light-sensitive transient receptor potential and transient receptor potential-like channels, even in norpA P24 , leading to the conclusion that this action was independent of PLC (Agam, K., von Campenhausen, M., Levy, S., Ben-Ami, H. C., Cook, B., Kirschfeld, K., and Minke, B. (2000) J. Neurosci. 20, 5748 -5755). However, we found that channel activation by metabolic inhibitors in norpA P24 was strictly dependent on the residual PLC activity underlying the spontaneous current, because the inhibitors failed to activate any channels after the spontaneous current had decayed. By contrast, polyunsaturated fatty acids invariably activated the channels independently of PLC. The results strongly support the obligatory requirement for PLC and DAG in Drosophila phototransduction, suggest that activation by metabolic inhibition is primarily because of the failure of diacylglycerol kinase, and are consistent with the proposal that polyunsaturated fatty acids, which are potential DAG metabolites, act directly on the channels.

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Section: Discussionsupporting

confidence: 80%

Section: Spontaneous Currents and Light Responses In Norpamentioning

confidence: 90%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Rescue of Light Responses in the Drosophila “Null” Phospholipase C Mutant, norpA, by the Diacylglycerol Kinase Mutant, rdgA, and by Metabolic Inhibition

Hardie

Martín

Chyb³

et al. 2003

Journal of Biological Chemistry

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Elements of Olfactory Reception in Adult Drosophila melanogaster

Martín

Boto

Gomez‐Diaz

et al. 2013

The Anatomical Record

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The olfactory system of Drosophila has become an attractive and simple model to investigate olfaction because it follows the same organizational principles of vertebrates, and the results can be directly applied to other insects with economic and sanitary relevance. Here, we review the structural elements of the Drosophila olfactory reception organs at the level of the cells and molecules involved. This article is intended to reflect the structural basis underlying the functional variability of the detection of an olfactory universe composed of thousands of odors. At the genetic level, we further detail the genes and transcription factors (TF) that determine the structural variability. The fly's olfactory receptor organs are the third antennal segments and the maxillary palps, which are covered with sensory hairs called sensilla. These sensilla house the odorant receptor neurons (ORNs) that express one or few odorant receptors in a stereotyped pattern regulated by combinations of TF. Also, perireceptor events, such as odor molecules transport to their receptors, are carried out by odorant binding proteins. In addition, the rapid odorant inactivation to preclude saturation of the system occurs by biotransformation and detoxification enzymes. These additional events take place in the lymph that surrounds the ORNs. We include some data on ionotropic and metabotropic olfactory transduction, although this issue is still under debate in Drosophila.

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Epithelial microRNA‐9a regulates dendrite growth through Fmi‐Gq signaling in Drosophila sensory neurons

Wang

et al. 2015

Developmental Neurobiology

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microRNA-9 (miR-9) is highly expressed in the nervous system across species and plays essential roles in neurogenesis and axon growth; however, little is known about the mechanisms that link miR-9 with dendrite growth. Using an in vivo model of Drosophila class I dendrite arborization (da) neurons, we show that miR-9a, a Drosophila homolog of mammalian miR-9, downregulates the cadherin protein Flamingo (Fmi) thereby attenuating dendrite development in a non-cell autonomous manner. In miR-9a knockout mutants, the dendrite length of a sensory neuron ddaE was significantly increased. Intriguingly, miR-9a is specifically expressed in epithelial cells but not in neurons, thus the expression of epithelial but not neuronal Fmi is greatly elevated in miR-9a mutants. In contrast, overexpression of Fmi in the neuron resulted in a reduction in dendrite growth, suggesting that neuronal Fmi plays a suppressive role in dendrite growth, and that increased epithelial Fmi might promote dendrite growth by competitively binding to neuronal Fmi. Fmi has been proposed as a G protein-coupled receptor (GPCR), we find that neuronal G protein Gαq (Gq), but not Go, may function downstream of Fmi to negatively regulate dendrite growth. Taken together, our results reveal a novel function of miR-9a in dendrite morphogenesis. Moreover, we suggest that Gq might mediate the intercellular signal of Fmi in neurons to suppress dendrite growth. Our findings provide novel insights into the complex regulatory mechanisms of microRNAs in dendrite development, and further reveal the interplay between the different components of Fmi, functioning in cadherin adhesion and GPCR signalling.

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Molecular Basis of Amplification in Drosophila Phototransduction

Cited by 108 publications

References 46 publications

Rescue of Light Responses in the Drosophila “Null” Phospholipase C Mutant, norpA, by the Diacylglycerol Kinase Mutant, rdgA, and by Metabolic Inhibition

Rescue of Light Responses in the Drosophila “Null” Phospholipase C Mutant, norpA, by the Diacylglycerol Kinase Mutant, rdgA, and by Metabolic Inhibition

Elements of Olfactory Reception in Adult Drosophila melanogaster

Epithelial microRNA‐9a regulates dendrite growth through Fmi‐Gq signaling in Drosophila sensory neurons

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