Involvement of the R2R3-MYB, AtMYB61, in the ectopic lignification and dark-photomorphogenic components of the det3 mutant phenotype
Involvement of the R2R3-MYB, AtMYB61, in the ectopic lignification and dark-photomorphogenic components of the det3 mutant phenotype
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DOI：
10.1046/j.1365-313x.2003.01953.x
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发表时间：
2004-01-01
期刊：
影响因子：
7.2
通讯作者：
Campbell, MM
中科院分区：
文献类型：
--
作者：
Newman, LJ;Perazza, DE;Campbell, MM
在拟南芥中，松树MYB PtMYB4的过度表达导致异位木质素沉积，并使植物即使在黑暗中生长也能进行光形态发生。PtMYB4过表达引起的表型与先前表征的暗光形态发生突变体deetiolated 3 （det3）相似；因此，我们验证了MYB错误表达可能解释det3表型的假设。我们在这里发现，拟南芥R2R3-MYB家族成员AtMYB61在det3突变体中错误表达。半定量逆转录聚合酶链反应（RT-PCR）实验表明，AtMYB61在det3背景下相对于野生型植物存在错误表达。在det3背景下对AtMYB61启动子活性的检测表明，AtMYB61表达的空间控制缺失。为了确定这种错误表达是否可以解释突变表型，AtMYB61在野生型拟南芥植物中过表达。过表达AtMYB61的转基因植株具有与det3突变体相同的异位木质化和暗光形态发生表型。为了检验AtMYB61是否在det3表型的这些方面是必需的，我们在反义和义抑制实验中下调了AtMYB61在det3植物中的表达。在det3突变背景下，抑制AtMYB61可以恢复与黑暗中发育相关的det3突变体的所有突变表型。综上所述，这些结果表明AtMYB61的错误表达是解释det3突变体异位木质化和暗光形态发生表型的充分和必要的。
Overexpression of a pine MYB, PtMYB4, in Arabidopsis caused ectopic lignin deposition and allowed the plants to undergo photomorphogenesis even when they were grown in the dark. The phenotype caused by PtMYB4 overexpression was reminiscent of the previously characterised dark-photomorphogenic mutant, de-etiolated 3 (det3); consequently, we tested the hypothesis that MYB misexpression may explain aspects of the det3 phenotype. We show here that AtMYB61, a member of the Arabidopsis R2R3-MYB family, is misexpressed in the det3 mutant. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) experiments suggested that AtMYB61 was misexpressed in a det3 background relative to wild-type plants. Examination of AtMYB61 promoter activity in a det3 background showed that the spatial control of AtMYB61 expression was lost. In order to determine if such misexpression could explain the mutant phenotype, AtMYB61 was overexpressed in wild-type Arabidopsis plants. Transgenic plants that overexpressed AtMYB61 had the same ectopic lignification and dark-photomorphogenic phenotype as that of the det3 mutant. In order to test if AtMYB61 was necessary for these aspects of the det3 phenotype, AtMYB61 expression was downregulated in det3 plants in both antisense and sense suppression experiments. Suppression of AtMYB61 in a det3 mutant background restored all mutant phenotypes of the det3 mutant associated with development in the dark. Taken together, these results suggest that AtMYB61 misexpression was both sufficient and necessary to explain the ectopic lignification and dark-photomorphogenic phenotypes of the det3 mutant.