背景回顾：Osmotic stress influences root system architecture, and polar auxin transport (PAT) is well-established to regulate root growth and development. 

提出问题：However, how PAT responds to osmotic stress at the molecular level remains poorly understood. 

主要研究：In this study, we explored whether and how the auxin efflux carrier PIN-FORMED3 (PIN3) participates in osmotic stress-induced root growth inhibition in Arabidopsis (Arabidopsis thaliana). 

结果1-渗透胁迫诱导HAT2基因表达：We observed that osmotic stress induces a HD-ZIP II transcription factor-encoding gene HOMEODOMAIN ARABIDOPSIS THALIANA2 (HAT2) expression in roots.

结果2-hat2功能缺失：The hat2 loss-of-function mutant is less sensitive to osmotic stress in terms of root meristem growth. Consistent with this phenotype, whereas the auxin response is down-regulated in wild-type roots under osmotic stress, the inhibition of auxin response by osmotic stress was alleviated in hat2 roots. 

结果3-HAT2过表达：Conversely, transgenic lines overexpressing HAT2 (Pro35S::HAT2) had shorter roots and reduced auxin accumulation compared with wild-type plants.

结果4-PIN3与HAT2：PIN3 expression was significantly reduced in the Pro35S::HAT2 lines. We determined that osmotic stress-mediated repression of PIN3 was alleviated in the hat2 mutant because HAT2 normally binds to the promoter of PIN3 and inhibits its expression.

结论：Taken together, our data reveal that osmotic stress inhibits root growth via HAT2, which regulates auxin activity by directly repressing PIN3 transcription.

 摘 要 

渗透胁迫影响植物根系统结构，而极性生长素运输是调控根生长和发育的关键因素。但是，极性生长素运输如何在分子层面响应于渗透胁迫还不清楚。本文中，作者研究了拟南芥生长素外流载体蛋白PIN3是否以及如何参与渗透胁迫介导的根生长抑制。作者发现渗透胁迫诱导了一个HD-ZIP II转录因子HAT2基因在根中的表达。同时，hat2突变体在根分生组织生长方面，对于渗透胁迫更加不敏感。与此表型一致的是，野生型拟南芥的根在渗透胁迫下生长素响应减弱，而在hat2突变体中渗透胁迫介导的生长素响应抑制状况有所缓解。相反，相比于野生型植株，HAT2过表达的株系具有更短的根，同时生长素的积累减少。在HAT2过表达株系中，PIN3基因的表达显著下降。作者发现，渗透胁迫介导的PIN3基因抑制之所以能够在 hat2突变体中有所缓解，是因为HAT2能够结合到PIN3的启动子上并抑制其表达。综上，本文的研究结果揭示了渗透胁迫诱导HAT2表达，而HAT2能够直接结合到PIN3基因的启动子上，抑制PIN3的表达，从而通过控制生长素的活性，抑制根的生长。