Ly Valentina, Collister David T, Fonseca Emerald, Liao Timothy S, Schroeder Dana F
Department of Biological Sciences, University of Manitoba, Winnipeg, MB R3T 2N2, Canada.
Department of Biological Sciences, University of Manitoba, Winnipeg, MB R3T 2N2, Canada.
Plant Sci. 2015 Feb;231:114-23. doi: 10.1016/j.plantsci.2014.11.011. Epub 2014 Dec 4.
de-etiolated 1 (det1) and constitutive photomorphogenic 1 (cop1) were initially identified as constitutively photomorphogenic Arabidopsis mutants, exhibiting light-grown phenotypes in the dark. Subsequently, both were shown to be components of Damaged DNA Binding protein 1 (DDB1)/CULLIN4-type complexes. Arabidopsis has two DDB1 homologues, DDB1A and DDB1B, and DDB1A mutants enhance det1 phenotypes. Here we examine ddb1a cop1 double mutants and find that ddb1a weakly enhances some cop1 phenotypes but not others, suggesting developmental regulation of COP1-DDB1A interaction. DET1 loss of function strongly enhances cop1 phenotypes. Here we show that MycDET1 overexpression also enhances cop1 phenotypes, thus MycDET1 overexpression in cop1 mutants also generates loss of function effects. Finally, the effect of the cop1 mutant background on the biochemical properties of MycDET1 was examined. MycDET1 levels were found to be lower in the dark than in the light and this difference required COP1. In summary, both DDB1A loss of function and MycDET1 overexpression enhance cop1 phenotypes, while cop1 mutants fail to exhibit light regulation of MycDET1 levels.
去黄化1（det1）和组成型光形态建成1（cop1）最初被鉴定为组成型光形态建成的拟南芥突变体，在黑暗中表现出光生长的表型。随后，两者都被证明是损伤DNA结合蛋白1（DDB1）/CULLIN4型复合物的组成部分。拟南芥有两个DDB1同源物，DDB1A和DDB1B，DDB1A突变体增强了det1的表型。在这里，我们研究了ddb1a cop1双突变体，发现ddb1a微弱地增强了一些cop1的表型，但不是其他表型，这表明COP1-DDB1A相互作用存在发育调控。DET1功能丧失强烈增强cop1表型。在这里我们表明，MycDET1的过表达也增强了cop1表型，因此在cop1突变体中MycDET1的过表达也产生了功能丧失效应。最后，研究了cop1突变体背景对MycDET1生化特性的影响。发现MycDET1水平在黑暗中比在光下低，这种差异需要COP1。总之，DDB1A功能丧失和MycDET1过表达都增强了cop1表型，而cop1突变体未能表现出对MycDET1水平的光调节。
