Arabidopsis AUXIN RESPONSE FACTOR6 and 8 Regulate Jasmonic Acid Biosynthesis and Floral Organ Development via Repression of Class 1 KNOX Genes
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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DOI：
10.1093/pcp/pcp176
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发表时间：
2010-01-01
影响因子：
4.9
通讯作者：
Ishiguro, Sumie
中科院分区：
文献类型：
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作者：
Tabata, Ryo;Ikezaki, Masaya;Ishiguro, Sumie
拟南芥中的两个突变，生长素反应因子6（arf6）和arf8，伴随着延迟花器官的伸长，随后延迟开放的花蕾。这种表型与茉莉酸（JA）缺陷突变体dad 1共享，并且，事实上，arf6 arf8花蕾的JA水平降低。在JA生物合成基因中，DAD 1（DEFECTIVE IN ANTHER DEHISCENCE1）的表达水平在双突变体中显著降低，表明ARF 6和ARF 8是激活DAD 1表达所必需的。双突变体arf 6和arf 8还表现出花的其他发育缺陷，如异常的维管图案和花瓣表皮细胞分化的缺乏。我们发现，1类KNOX基因异位表达在arf6 arf8的花器官发育，和任何1类KNOX基因（knat2，knat6，bp和半合子stm）的突变部分抑制缺陷的双突变体。此外，STM基因的异位表达引起与arf6 arf8相似的表型，包括DAD 1表达的下调。这些结果表明，arf 6和arf 8中的大多数缺陷可归因于1类KNOX基因的异常表达。在arf6 arf8花中，AS 1和AS 2的表达不受影响，并且AS 1和arf6 arf8相加地增加了1类KNOX基因的表达。我们的结论是，ARF6和ARF8，与AS1和AS2平行，抑制类1 KNOX基因在发展中的花器官，使这些器官的发展进程。
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.