Nitric oxide feedback to ciliary photoreceptor cells gates a UV avoidance circuit

Nitric oxide feedback to ciliary photoreceptor cells gates a UV avoidance circuit
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一氧化氮反馈到睫状感光细胞控制紫外线避免电路

DOI:
10.1101/2023.08.02.551600
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发表时间:
2023
期刊:
--
影响因子:
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通讯作者:
Jokura K
Jokura K
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--
文献类型:
--
作者:
Jokura K

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一氧化氮合酶(NOS)产生的一氧化氮(NO)是动物生理的重要调节因子。在这里,我们揭示了一个功能NO在紫外线曝光和紫外线避免电路的门控集成。研究了脑睫状光感受器(cPRCs)介导的杜氏扁虫(Platynereis dumerilii)幼虫对紫外线/紫光的回避作用。在幼虫中,NOS在cPRC突触后的中间神经元(INNOS)中表达。UV刺激cPRC触发INNOS激活和NO产生。NO信号逆行cPRC诱导其持续的刺激后激活,通过非常规的鸟苷酸环化酶。这种晚期激活抑制了多巴胺能纤毛神经元诱导向下游泳。InNOS突变体、逆行信号传导、电路输出和UV回避是有缺陷的。通过数学建模,我们概括了野生型和突变幼虫的光转导和电路动力学。我们的研究结果揭示了如何NO介导的逆行信号门突触电路,并诱导短期记忆的紫外线暴露,以协调光回避行为。
Nitric oxide (NO) produced by nitric-oxide synthase (NOS) is a key regulator of animal physiology. Here we uncover a function for NO in the integration of UV exposure and the gating of a UV-avoidance circuit. We studied UV/violet avoidance mediated by brain ciliary photoreceptors (cPRCs) in larvae of the annelidPlatynereis dumerilii. In the larva, NOS is expressed in interneurons (INNOS) postsynaptic to cPRCs. UV stimulation of cPRCs triggers INNOS activation and NO production. NO signals retrogradely to cPRCs to induce their sustained post-stimulus activation through an unconventional guanylate cyclase. This late activation inhibits serotonergic ciliomotor neurons to induce downward swimming. InNOSmutants, retrograde signalling, circuit output and UV avoidance are defective. By mathematical modelling, we recapitulate phototransduction and circuit dynamics in wild-type and mutant larvae. Our results reveal how NO-mediated retrograde signalling gates a synaptic circuit and induces short-term memory of UV exposure to orchestrate light-avoidance behaviour.
关于一氧化氮合酶的新见解,并且在海藻变态中没有信号传导。
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