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1
Mutations in a C. elegans Gqalpha gene disrupt movement, egg laying, and viability.秀丽隐杆线虫Gqα基因的突变会破坏运动、产卵和生存能力。
Neuron. 1996 May;16(5):999-1009. doi: 10.1016/s0896-6273(00)80123-3.
2
Caenorhabditis elegans Galphaq regulates egg-laying behavior via a PLCbeta-independent and serotonin-dependent signaling pathway and likely functions both in the nervous system and in muscle.秀丽隐杆线虫的Gαq通过一条不依赖磷脂酶Cβ(PLCβ)且依赖血清素的信号通路调节产卵行为,并且可能在神经系统和肌肉中都发挥作用。
Genetics. 2003 Dec;165(4):1805-22. doi: 10.1093/genetics/165.4.1805.
3
Activation of EGL-47, a Galpha(o)-coupled receptor, inhibits function of hermaphrodite-specific motor neurons to regulate Caenorhabditis elegans egg-laying behavior.EGL-47(一种与Gα(o)偶联的受体)的激活会抑制雌雄同体特异性运动神经元的功能,从而调节秀丽隐杆线虫的产卵行为。
J Neurosci. 2004 Sep 29;24(39):8522-30. doi: 10.1523/JNEUROSCI.1915-04.2004.
4
Participation of the protein Go in multiple aspects of behavior in C. elegans.蛋白质Go参与秀丽隐杆线虫行为的多个方面。
Science. 1995 Mar 17;267(5204):1652-5. doi: 10.1126/science.7886455.
5
Opposing functions of calcineurin and CaMKII regulate G-protein signaling in egg-laying behavior of C.elegans.钙调神经磷酸酶和钙/钙调蛋白依赖性蛋白激酶II的相反功能调节秀丽隐杆线虫产卵行为中的G蛋白信号传导。
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6
EGL-36 Shaw channels regulate C. elegans egg-laying muscle activity.EGL-36 Shaw通道调节秀丽隐杆线虫的产卵肌肉活动。
Neuron. 1997 Jul;19(1):165-74. doi: 10.1016/s0896-6273(00)80356-6.
7
Egg-laying defective mutants of the nematode Caenorhabditis elegans.线虫秀丽隐杆线虫的产卵缺陷突变体。
Genetics. 1983 Aug;104(4):619-47. doi: 10.1093/genetics/104.4.619.
8
Two RGS proteins that inhibit Galpha(o) and Galpha(q) signaling in C. elegans neurons require a Gbeta(5)-like subunit for function.在秀丽隐杆线虫神经元中抑制Gα(o)和Gα(q)信号传导的两种RGS蛋白发挥功能需要一个类Gβ(5)亚基。
Curr Biol. 2001 Feb 20;11(4):222-31. doi: 10.1016/s0960-9822(01)00071-9.
9
Multiple RGS proteins alter neural G protein signaling to allow C. elegans to rapidly change behavior when fed.多种RGS蛋白改变神经G蛋白信号传导,使秀丽隐杆线虫在进食时能迅速改变行为。
Genes Dev. 2000 Aug 15;14(16):2003-14.
10
egl-17 encodes an invertebrate fibroblast growth factor family member required specifically for sex myoblast migration in Caenorhabditis elegans.egl-17编码一种无脊椎动物成纤维细胞生长因子家族成员,该成员是秀丽隐杆线虫中性肌母细胞迁移所特需的。
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2433-7. doi: 10.1073/pnas.94.6.2433.

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Regulation of Diacylglycerol Content in Olfactory Neurons Determines Forgetting or Retrieval of Olfactory Memory in .调节嗅神经元中二酰基甘油含量决定嗅觉记忆的遗忘或提取。
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Serotonin signals through postsynaptic Gαq, Trio RhoGEF, and diacylglycerol to promote Caenorhabditis elegans egg-laying circuit activity and behavior.血清素通过突触后 Gαq、Trio RhoGEF 和二酰基甘油传递信号,促进秀丽隐杆线虫产卵回路活动和行为。
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Co-transmission of neuropeptides and monoamines choreograph the C. elegans escape response.神经肽和单胺类递质的共传递协调秀丽隐杆线虫的逃避反应。
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本文引用的文献

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Toward a physical map of the genome of the nematode Caenorhabditis elegans.构建秀丽隐杆线虫基因组物理图谱。
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Egg-laying defective mutants of the nematode Caenorhabditis elegans.线虫秀丽隐杆线虫的产卵缺陷突变体。
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Gene structure of murine Gna11 and Gna15: tandemly duplicated Gq class G protein alpha subunit genes.小鼠Gna11和Gna15的基因结构:串联重复的Gq类G蛋白α亚基基因。
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Interacting genes required for pharyngeal excitation by motor neuron MC in Caenorhabditis elegans.秀丽隐杆线虫中运动神经元MC引起咽部兴奋所需的相互作用基因。
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Analysis of dominant mutations affecting muscle excitation in Caenorhabditis elegans.秀丽隐杆线虫中影响肌肉兴奋的显性突变分析。
Genetics. 1995 Nov;141(3):961-76. doi: 10.1093/genetics/141.3.961.
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The 2.0 A crystal structure of a heterotrimeric G protein.异源三聚体G蛋白的2.0埃晶体结构。
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7
EGL-10 regulates G protein signaling in the C. elegans nervous system and shares a conserved domain with many mammalian proteins.EGL-10在秀丽隐杆线虫神经系统中调节G蛋白信号传导,并与许多哺乳动物蛋白共享一个保守结构域。
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The genetics of feeding in Caenorhabditis elegans.秀丽隐杆线虫进食行为的遗传学研究
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9
Motor neuron M3 controls pharyngeal muscle relaxation timing in Caenorhabditis elegans.运动神经元M3控制秀丽隐杆线虫咽部肌肉的松弛时间。
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10
Splicing in Caenorhabditis elegans does not require an AG at the 3' splice acceptor site.秀丽隐杆线虫中的剪接在3'剪接受体位点不需要AG。
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秀丽隐杆线虫Gqα基因的突变会破坏运动、产卵和生存能力。

Mutations in a C. elegans Gqalpha gene disrupt movement, egg laying, and viability.

作者信息

Brundage L, Avery L, Katz A, Kim U J, Mendel J E, Sternberg P W, Simon M I

机构信息

Division of Biology and Howard Hughes Medical Institute of Technology, Pasadena, California 91125, USA.

出版信息

Neuron. 1996 May;16(5):999-1009. doi: 10.1016/s0896-6273(00)80123-3.

DOI:10.1016/s0896-6273(00)80123-3
PMID:8630258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4444781/
Abstract

We find that C. elegans egl-30 encodes a heterotrimeric G protein a subunit more than 80% identical to mammalian Gqalpha family proteins, and which can function as a Gqalpha subunit in COS-7 cells. We have identified new egl-30 alleles in a selection for genes involved in the C. elegans acetylcholine response. Two egl-30 alleles specify premature termination of Gqalpha and are essentially lethal in homozygotes. Animals homozygous for six other egl-30 alleles are viable and fertile, but exhibit delayed egg laying and leave flattened tracks. Overexpression of the wild-type egl-30 gene produces the opposite behavior. Analysis of these mutants suggest that their phenotypes reflect defects in the muscle or neuromuscular junction.

摘要

我们发现,秀丽隐杆线虫的egl-30编码一种异源三聚体G蛋白α亚基,与哺乳动物Gqα家族蛋白的同源性超过80%,并且在COS-7细胞中可作为Gqα亚基发挥作用。我们在筛选参与秀丽隐杆线虫乙酰胆碱反应的基因时鉴定出了新的egl-30等位基因。两个egl-30等位基因导致Gqα提前终止,纯合子基本致死。其他六个egl-30等位基因的纯合动物可存活且可育,但产卵延迟且留下扁平的轨迹。野生型egl-30基因的过表达则产生相反的行为。对这些突变体的分析表明,它们的表型反映了肌肉或神经肌肉接头的缺陷。