首页> 外文期刊>Plant and cell physiology >Arabidopsis AUXIN RESPONSE FACTOR6 and 8 regulate jasmonic acid biosynthesis and floral organ development via repression of class 1 KNOX genes.
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Arabidopsis AUXIN RESPONSE FACTOR6 and 8 regulate jasmonic acid biosynthesis and floral organ development via repression of class 1 KNOX genes.

机译:拟南芥 AUXIN响应因子6和8通过抑制1类 KNOX 基因来调节茉莉酸的生物合成和花器官发育。

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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.
机译:拟南芥的两个突变,生长素反应因子6 ( arf6 )和 arf8 ,同时延迟了花器官的伸长随后推迟了花蕾的开放。该表型与缺乏茉莉酸(JA)的突变体 dad1 共享,实际上, arf6 arf8 花芽的JA水平降低了。在JA生物合成基因中,双突变体中 DAD1 (花药在花药中的缺陷)的表达水平显着降低,表明 ARF6 和<激活 DAD1 表达需要i> ARF8 。双重突变体 arf6 arf8 还显示了花朵的其他发育缺陷,例如异常的血管模式和花瓣中缺乏表皮细胞分化。我们发现1类 KNOX 基因在 arf6 arf8 发育中的花器官中异位表达,并且任何1类 KNOX 基因均发生突变( knat2 , knat6 , bp 和半合子 stm )部分地抑制了双突变体中的缺陷。此外, STM 基因的异位表达导致与 arf6 arf8 相似的表型,包括 DAD1 表达的下调。这些结果表明, arf6 arf8 中的大多数缺陷都归因于1类 KNOX 基因的异常表达。 AS1 和 AS2 的表达在 arf6 arf8 花以及 as1 和 arf6 arf8花中均不受影响增加了1类 KNOX 基因的表达。我们得出的结论是,ARF6和ARF8与AS1和AS2平行,在发育中的花器官中抑制1类 KNOX 基因,从而允许这些器官的发育进程。

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