Genetic interactions between the chlorate-resistant mutant cr88 and the photomorphogenic mutants cop1 and hy5
Genetic interactions between the chlorate-resistant mutant cr88 and the photomorphogenic mutants cop1 and hy5
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DOI：
10.1105/tpc.12.2.199
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发表时间：
2000-02-01
期刊：
影响因子：
11.6
通讯作者：
Cheng, CL
中科院分区：
文献类型：
--
作者：
Cao, D;Lin, Y;Cheng, CL
从红光和黄子叶在所有光照条件下的长下胚轴的表型可以看出，抗氯酸盐突变体cr88在光形态发生方面存在缺陷。在cr88中，光调控基因的一个子集的表达水平低于正常水平。为了进一步分析CR88在光形态建成中的作用，我们研究了CR88与另外两个影响光形态建成的基因位点的遗传互作，这两个基因是结构性光形态建成基因1(COP1)和长下胚光形态建成基因5(HY5)。COP1在黑暗中抑制光调节基因的表达，HY5在光中抑制下胚轴的伸长。使用形态、细胞和基因表达标准进行上位性分析，将CR88定位在光形态建成途径的遗传层次中，我们确定CR88作用于COP1下游，但位于与HY5分开的一个分支中。在我们的分析过程中，我们发现光线会导致黑暗生长的Cop1幼苗中的叶绿体被广泛破坏，而cr88可以阻止这种破坏。
The chlorate-resistant mutant cr88 is defective in photomorphogenesis, as shown by the phenotypes of long hypocotyls in red light and yellow cotyledons under all light conditions. A subset of light-regulated genes is expressed at subnormal levels in cr88. To analyze further the role that CR88 plays in photomorphogenesis, we investigated the genetic interactions between cr88 and mutants of two other loci affecting photomorphogenesis, CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) and LONG HYPOCOTYL5 (HY5). COP1 represses the expression of light-regulated genes in the dark, and HY5 inhibits hypocotyl elongation in the light. Using morphological, cellular, and gene expression criteria for epistasis analyses to position CR88 in the genetic hierarchy of the photomorphogenesis pathway, we determined that CR88 acts downstream of COP1 but in a branch separate from HY5. in the course of our analysis, we discovered that light causes extensive destruction of plastids in dark-grown cop1 seedlings and that cr88 prevents this destruction.