Shteingauz Anna, Cohen Emiliano, Biala Yoav, Treinin Millet
Department of Physiology, Hebrew University, Hadassah Medical School, Jerusalem, 91120, Israel.
J Cell Sci. 2009 Mar 15;122(Pt 6):807-12. doi: 10.1242/jcs.036343. Epub 2009 Feb 17.
RIC-3 is a member of a conserved family of proteins that affect nicotinic acetylcholine receptor maturation. In yeast and in vitro, BATH-42, a BTB- and MATH-domain-containing protein, interacts with RIC-3. BATH-42 is also known to interact with the CUL-3 ubiquitin ligase complex. Loss of BATH-42 function leads to increased RIC-3 expression and decreased activity of nicotinic acetylcholine receptors in Caenorhabditis elegans vulva muscles. Increased expression of RIC-3 is deleterious for activity and distribution of nicotinic acetylcholine receptors, and thus the effects of BATH-42 loss of function on RIC-3 expression explain the associated reduction in receptor activity. Overexpression of BATH-42 is also detrimental to nicotinic acetylcholine receptor function, leading to decreased pharyngeal pumping. This effect depends on the C-terminus of RIC-3 and on CUL-3. Thus, our work suggests that BATH-42 targets RIC-3 to degradation via CUL-3-mediated ubiquitylation. This demonstrates the importance of regulation of RIC-3 levels, and identifies a mechanism that protects cells from the deleterious effects of excess RIC-3.
RIC-3是影响烟碱型乙酰胆碱受体成熟的保守蛋白家族成员。在酵母和体外实验中,含BTB和MATH结构域的蛋白BATH-42与RIC-3相互作用。已知BATH-42也与CUL-3泛素连接酶复合物相互作用。秀丽隐杆线虫外阴肌肉中BATH-42功能缺失会导致RIC-3表达增加,烟碱型乙酰胆碱受体活性降低。RIC-3表达增加对烟碱型乙酰胆碱受体的活性和分布有害,因此BATH-42功能缺失对RIC-3表达的影响解释了受体活性相关的降低。BATH-42的过表达对烟碱型乙酰胆碱受体功能也有害,导致咽部抽吸减少。这种效应取决于RIC-3的C末端和CUL-3。因此,我们的研究表明BATH-42通过CUL-3介导的泛素化将RIC-3靶向降解。这证明了调节RIC-3水平的重要性,并确定了一种保护细胞免受过量RIC-3有害影响的机制。