Genetic linkages between circadian clock-associated components and phytochrome-dependent red light signal transduction in Arabidopsis thaliana
Genetic linkages between circadian clock-associated components and phytochrome-dependent red light signal transduction in Arabidopsis thaliana
复制标题
DOI：
10.1093/pcp/pcm063
复制
发表时间：
2007-07-01
影响因子：
4.9
通讯作者：
Mizuno, Takeshi
中科院分区：
文献类型：
--
作者：
Ito, Shogo;Nakamichi, Norihito;Mizuno, Takeshi
目前拟南芥时钟成分的最佳候选基因是CCA1 （CIRCADIAN clock - associated 1）及其同源基因LHY （LATE ELONGATED HYPOCOTYL）。此外，一个小家族的五个成员伪响应调节器（包括PRR1， PRR3, PRR5， PRR7和PRR9）被认为是另一种类型的时钟组件。最初描述的PRRs成员是TOC1（或PRR1） （CAB表达的时间1）。有趣的是，携带特定时钟相关基因损伤（即功能丧失或错误表达）的拟南藓幼苗在早期光形态形成过程中通常表现出光响应的特征表型。例如，在一定的红光照射率下（即对红光过敏），cca1 - hy双突变苗的下胚轴长度比野生型短。而下胚轴较长的toc1单突变体和prr7 prr5双突变体幼苗在相同条件下均表现为低敏感性。这些表型表明昼夜节律钟和红光信号转导机制之间存在联系。在这里，通过对大量携带时钟相关基因病变的突变体和转基因系进行组合遗传和显性分析，解决了这个问题，这些突变体和转基因系包括cca1 lhy toc1三重突变体和cca1 lhy prr7 prr5四倍突变体。综合这些结果，我们提出了一个时钟相关红光信号的遗传模型，其中CCA1和LHY在TOC1 （PRR1）上游以负向方式发挥作用，而TOC1 （PRR1）则作为正向调节因子。PRR7和PRR5也作为正调控因子，但独立于TOC1 （PRR1）。进一步表明，这些信号通路协调整合到光敏色素介导的红光信号转导通路中，其中PIF3（光敏色素相互作用因子3）作为phyB下游的负调节因子发挥作用。
The current best candidates for Arabidopsis thaliana clock components are CCA1 ( CIRCADIAN CLOCK-ASSOCIATED 1) and its homolog LHY ( LATE ELONGATED HYPOCOTYL). In addition, five members of a small family, PSEUDO- RESPONSE REGULATORS ( including PRR1, PRR3, PRR5, PRR7 and PRR9), are believed to be another type of clock component. The originally described member of PRRs is TOC1 ( or PRR1) ( TIMING OF CAB EXPRESSION 1). Interestingly, seedlings of A. thaliana carrying a certain lesion ( i. e. loss- of- function or misexpression) of a given clock- associated gene commonly display a characteristic phenotype of light response during early photomorphogenesis. For instance, cca1 lhy double mutant seedlings show a shorter hypocotyl length than the wild type under a given fluence rate of red light ( i. e. hypersensitivity to red light). In contrast, both toc1 single and prr7 prr5 double mutant seedlings with longer hypocotyls are hyposensitive under the same conditions. These phenotypes are indicative of linkage between the circadian clock and red light signal transduction mechanisms. Here this issue was addressed by conducting combinatorial genetic and epistasis analyses with a large number of mutants and transgenic lines carrying lesions in clock- associated genes, including a cca1 lhy toc1 triple mutant and a cca1 lhy prr7 prr5 quadruple mutant. Taking these results together, we propose a genetic model for clock- associated red light signaling, in which CCA1 and LHY function upstream of TOC1 ( PRR1) in a negative manner, in turn, TOC1 ( PRR1) serves as a positive regulator. PRR7 and PRR5 also act as positive regulators, but independently from TOC1 ( PRR1). It is further suggested that these signaling pathways are coordinately integrated into the phytochrome- mediated red light signal transduction pathway, in which PIF3 ( PHYTOCHROME- INTERACTING FACTOR 3) functions as a negative regulator immediately downstream of phyB.