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Class I TCP proteins TCP14 and TCP15 are required for elongation and gene expression responses to auxin

生长素 生物 突变体 基因表达 延伸率 野生型 基因 转录因子 细胞生物学 发起人 下胚轴 抄写(语言学) 拟南芥 分子生物学 基因表达调控 遗传学 植物 语言学 材料科学 哲学 冶金 极限抗拉强度
作者
Lucía Ferrero,Victoria Gastaldi,Federico Ariel,Ivana L. Viola,Daniel H. González
出处
期刊:Plant Molecular Biology [Springer Science+Business Media]
卷期号:105 (1-2): 147-159 被引量:41
标识
DOI:10.1007/s11103-020-01075-y
摘要

Two class I TCP transcription factors are required for an efficient elongation of hypocotyls in response to auxin and for the correct expression of a subset of auxin-inducible genes In this work, we analyzed the response to auxin of plants with altered function of the class I TEOSINTE BRANCHED 1, CYCLOIDEA, PCF (TCP) transcription factors TCP14 and TCP15. Several SMALL AUXIN UP RNA (SAUR) genes showed decreased expression in mutant plants defective in these TCPs after an increase in ambient temperature to 29 °C, a condition that causes an increase in endogenous auxin levels. Overexpression of SAUR63 caused a more pronounced elongation response in the mutant than in the wild-type at 29 °C, suggesting that the decreased expression of SAUR genes is partly responsible for the defective elongation at warm temperature. Notably, several SAUR genes and the auxin response gene IAA19 also showed reduced expression in the mutant after auxin treatment, while the expression of other SAUR genes and of IAA29 was not affected or was even higher. Expression of the auxin reporter DR5::GUS was also higher in a tcp15 mutant than in a wild-type background after auxin treatment. However, the elongation of hypocotyls in response to auxin was impaired in the mutant. Remarkably, a significant proportion of auxin inducible genes and of targets of the AUXIN RESPONSE FACTOR 6 are regulated by TCP15 and often contain putative TCP recognition motifs in their promoters. Furthermore, we demonstrated that several among them are recognized by TCP15 in vivo. Our results indicate that TCP14 and TCP15 are required for an efficient elongation response to auxin, most likely by regulating a subset of auxin inducible genes related to cell expansion.
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