KAI2 regulates seedling development by mediating light-induced remodelling of auxin transport
KAI2 regulates seedling development by mediating light-induced remodelling of auxin transport
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KAI2 通过介导光诱导的生长素运输重塑来调节幼苗发育
DOI：
10.1101/2021.05.06.443001
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Hamon-Josse M
中科院分区：
文献类型：
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作者：
Hamon-Josse M
幼苗生长的光形态重塑是植物生命周期中一个关键的发育转变。α/β水解酶信号蛋白KARRIKIN - INSENSITIVE2 （KAI2）是独角麦内酯受体DWARF14 （D14）的密切同源物，参与了这一过程，但KAI2对发育的影响是如何介导的尚不清楚。通过对拟南芥（Heynh.）的生理、药理学、遗传和成像方法的综合研究，我们发现kai2表型的产生是由于未能下调从幼苗茎尖到根系的生长素运输，而不是未能对光照本身作出反应。我们证明KAI2控制光诱导的幼苗中PIN介导的生长素运输系统的重塑，促进衰老组织中PIN7丰度的降低，以及根分生组织中PIN1/PIN2丰度的增加。我们发现，从kai2突变体中去除PIN3、PIN4和PIN7，或药理抑制生长素的运输和合成，足以抑制大多数kai2幼苗表型。我们认为KAI2通过对生长素运输系统的影响来调控幼苗形态发生。我们提出KAI2不是光介导的PIN基因表达变化所必需的，但却是细胞内PIN蛋白丰度适当变化所必需的。
Photomorphogenic remodelling of seedling growth is a key developmental transition in the plant life cycle. The α/β‐hydrolase signalling protein KARRIKIN‐INSENSITIVE2 (KAI2), a close homologue of the strigolactone receptor DWARF14 (D14), is involved in this process, but it is unclear how the effects of KAI2 on development are mediated.Here, using a combination of physiological, pharmacological, genetic and imaging approaches inArabidopsis thaliana(Heynh.) we show thatkai2phenotypes arise because of a failure to downregulate auxin transport from the seedling shoot apex towards the root system, rather than a failure to respond to lightper se.We demonstrate that KAI2 controls the light‐induced remodelling of the PIN‐mediated auxin transport system in seedlings, promoting a reduction in PIN7 abundance in older tissues, and an increase of PIN1/PIN2 abundance in the root meristem. We show that removing PIN3, PIN4 and PIN7 fromkai2mutants, or pharmacological inhibition of auxin transport and synthesis, is sufficient to suppress mostkai2seedling phenotypes.We conclude that KAI2 regulates seedling morphogenesis by its effects on the auxin transport system. We propose that KAI2 is not required for the light‐mediated changes in PIN gene expression but is required for the appropriate changes in PIN protein abundance within cells.