Department of Biological Mechanisms and Functions, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Plant Cell Physiol. 2010 Jan;51(1):164-75. doi: 10.1093/pcp/pcp176. Epub 2009 Dec 10.
Two mutations in Arabidopsis thaliana, auxin response factor6 (arf6) and arf8, concomitantly delayed the elongation of floral organs and subsequently delayed the opening of flower buds. This phenotype is shared with the jasmonic acid (JA)-deficient mutant dad1, and, indeed, the JA level of arf6 arf8 flower buds was decreased. Among JA biosynthetic genes, the expression level of DAD1 (DEFECTIVE IN ANTHER DEHISCENCE1) was markedly decreased in the double mutant, suggesting that ARF6 and ARF8 are required for activation of DAD1 expression. The double mutant arf6 arf8 also showed other developmental defects in flowers, such as aberrant vascular patterning and lack of epidermal cell differentiation in petals. We found that class 1 KNOX genes were expressed ectopically in the developing floral organs of arf6 arf8, and mutations in any of the class 1 KNOX genes (knat2, knat6, bp and hemizygous stm) partially suppressed the defects in the double mutant. Furthermore, ectopic expression of the STM gene caused a phenotype similar to that of arf6 arf8, including the down-regulation of DAD1 expression. These results suggested that most defects in arf6 arf8 are attributable to abnormal expression of class 1 KNOX genes. The expression of AS1 and AS2 was not affected in arf6 arf8 flowers, and as1 and arf6 arf8 additively increased the expression of class 1 KNOX genes. We concluded that ARF6 and ARF8, in parallel with AS1 and AS2, repress the class 1 KNOX genes in developing floral organs to allow progression of the development of these organs.
拟南芥中的两个突变体，生长素反应因子 6（arf6）和 arf8，同时延迟了花器官的伸长，随后延迟了花蕾的开放。这种表型与茉莉酸（JA）缺陷突变体 dad1 共享，事实上，arf6 arf8 花蕾中的 JA 水平降低。在 JA 生物合成基因中，DAD1（花药开裂缺陷 1）的表达水平在双突变体中明显降低，表明 ARF6 和 ARF8 是激活 DAD1 表达所必需的。arf6 arf8 双突变体在花中也表现出其他发育缺陷，如花器官异常血管模式和花瓣缺乏表皮细胞分化。我们发现，类 1 KNOX 基因在 arf6 arf8 发育中的花器官中异位表达，并且任何类 1 KNOX 基因（knat2、knat6、bp 和半合子 stm）的突变都部分抑制了双突变体的缺陷。此外，STM 基因的异位表达导致类似于 arf6 arf8 的表型，包括 DAD1 表达的下调。这些结果表明，arf6 arf8 的大多数缺陷归因于类 1 KNOX 基因的异常表达。arf6 arf8 花中的 AS1 和 AS2 的表达不受影响，并且 as1 和 arf6 arf8 累加性地增加了类 1 KNOX 基因的表达。我们得出结论，ARF6 和 ARF8 与 AS1 和 AS2 平行，在发育中的花器官中抑制类 1 KNOX 基因的表达，以允许这些器官的发育进程。
