Hsieh H L, Okamoto H, Wang M, Ang L H, Matsui M, Goodman H, Deng X W
Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06520-8104 USA.
Genes Dev. 2000 Aug 1;14(15):1958-70.
Light signals perceived by photoreceptors are transduced to negatively regulate COP1, a key repressor of photomorphogenic development. To identify genes involved in light inactivation of COP1, a genetic screen was employed to identify extragenic modifier mutations of a temperature-sensitive cop1 allele. One suppressor mutation isolated also exhibited a far-red-specific long hypocotyl phenotype in a wild-type background. Further phenotypic analyses of this new mutation, named fin219, suggested that it defines a novel phytochrome A signaling component. Genetic analysis indicated that FIN219 interacts closely with another phytochrome A signaling component, FHY1. Molecular characterization of FIN219 indicated that it encodes a cytoplasmic localized protein highly similar to the GH3 family of proteins and its expression is rapidly induced by auxin. In contrast to its loss-of-function mutant phenotype, overexpression of FIN219 results in a far-red-specific hyperphotomorphogenic response. Our data suggest that FIN219 may define a critical link for phytochrome A-mediated far-red inactivation of COP1 and a possible cross-talk juncture between auxin regulation and phytochrome signaling.
光感受器感知的光信号被转导，以负向调节COP1，COP1是光形态建成发育的关键抑制因子。为了鉴定参与COP1光失活的基因，采用了遗传筛选来鉴定温度敏感型cop1等位基因的基因外修饰突变。分离出的一个抑制突变在野生型背景下也表现出远红光特异性的长下胚轴表型。对这个名为fin219的新突变的进一步表型分析表明，它定义了一个新的光敏色素A信号组分。遗传分析表明，FIN219与另一个光敏色素A信号组分FHY1密切相互作用。FIN219的分子特征表明，它编码一种定位于细胞质的蛋白质，与GH3蛋白家族高度相似，其表达受生长素快速诱导。与其功能缺失突变体表型相反，FIN219的过表达导致远红光特异性的超光形态建成反应。我们的数据表明，FIN219可能定义了光敏色素A介导的COP1远红光失活的关键环节，以及生长素调节和光敏色素信号之间可能的相互作用节点。
