FLP-1 neuropeptides modulate sensory and motor circuits in the nematode &ITCaenorhabditis elegans &IT
FLP-1 neuropeptides modulate sensory and motor circuits in the nematode &ITCaenorhabditis elegans &IT
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DOI：
10.1371/journal.pone.0189320
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发表时间：
2018-01-02
期刊：
影响因子：
3.7
通讯作者：
Li, Chris
中科院分区：
文献类型：
--
作者：
Buntschuh, Ingrid;Raps, Daniel A.;Li, Chris
寄生线虫感染了全世界四分之一以上的人口，导致超过十亿人发病。由于耐药菌株的存在，目前的驱虫药开始失去效力。我们对神经肽的作用感兴趣，神经肽调节所有生物体的行为，作为驱虫药的另一个可能靶标。 FMRF酰胺相关肽 (FaRP) 是整个动物界保守的神经肽家族。特别是，线虫包含迄今为止发现的最大的 FaRP 家族，并且其中许多 FaRP 在不同线虫物种中是相同的；线虫中的 FaRP 统称为 FLP（FMRFamide 样肽）。然而，人们对这些 FLP 的功能知之甚少。我们使用非寄生线虫秀丽隐杆线虫作为检查线虫 FLP 的模型。线虫包含至少 31 个 flp 基因，编码 72 个潜在的 FLP。在线虫中普遍存在的 flp 基因中，flp-1 是少数几个普遍存在的基因之一。此前有报道称 FLP-1 神经肽参与感觉和运动功能。然而，之前的 flp-1 等位基因也破坏了邻近的基因 daf-10。为了了解 flp-1 的表型，对特异性破坏 flp-1 的新等位基因进行了表征。先前报道的运动和产蛋缺陷被发现是由于 flp-1 的缺失，而渗透压缺陷是由于 daf-10 的缺失。此外，flp-1和daf-10的缺失都会导致几种表型，通过破坏神经回路中的不同神经元，使双突变体的严重程度增加。
Parasitic nematodes infect over one quarter of the population worldwide, causing morbidity in over one billion people. Current anthelmintic drugs are beginning to lose effectiveness due to the presence of resistant strains. We are interested in the role of neuropeptides, which regulate behaviors in all organisms, as another possible target for anthelmintic drugs. FMRFamide-related peptides (FaRPs) are a family of neuropeptides that are conserved throughout the animal kingdom. In particular, nematodes contain the largest family of FaRPs identified thus far and many of these FaRPs are identical among different nematode species; FaRPs in nematodes are collectively referred to as FLPs (FMRFamide-like peptides). However, little is known about the function of these FLPs. We are using the non-parasitic nematode Caenorhabditis elegans as a model for examining FLPs in nematodes. C. elegans contains at least 31 flp genes that encode 72 potential FLPs. Among the flp genes, flp-1 is one of the few that is universally found in nematodes. FLP-1 neuropeptides were previously reported to be involved in sensory and motor functions. However, previous alleles of flp-1 also disrupted a neighboring gene, daf-10. To understand the phenotypes of flp-1, new alleles that specifically disrupt flp-1 were characterized. The previously reported locomotory and egg-laying defects were found to be due to loss of flp-1, while the osmolarity defect is due to loss of daf-10. In addition, loss of flp-1 and daf-10 both cause several phenotypes that increase in severity in the double mutants by disrupting different neurons in the neural circuits.