高等植物的地上部分由茎尖分生组织（SAM）发育而来。SAM的活性是如何受到精细调控是植物发育生物学中一个十分重要的问题。最新的研究发现转录因子HAM可以通过和调控SAM活性的主要调节子WUS相互作用来调控维持SAM的活性。然而HAM本身又是如何被调控的尚有待进一步探究。拟南芥中，转录因子PHR1及其同源蛋白PHL1（PHR1-like 1），PHL2，PHL3是调控植物对低磷胁迫转录响应的主要调节子。我们前期的工作发现，phl2phl3双突变体其地上部分生长缓慢，发育延迟，其中大量和调控SAM活性相关的基因表达发生异常。我们进一步发现PHL3和HAM有直接的蛋白相互作用。本项目将综合运用多学科手段，来研究PHL2和PHL3是如何通过和HAM蛋白相互作用来调控SAM的活性。本项目获得的研究结果对进一步深入了解调控SAM活性的分子机制具有重要意义。

The aboveground parts of higher plants are derived from shoot apical meristem (SAM), and how the activity of SAM is maintained is an important question in plant developmental biology. . Recently, HAM family proteins were shown to interact with the key regulator of SAM, WUS, to regulate the SAM activity. However, how the function of HAMs is regulated by other factors remains unclear. Under phosphate deficiency, plants exhibit a dramatic change of transcriptomes to cope with this nutritional stress. The transcription factors PHR1 and PHR1-like proteins (PHL1, PHL2, PHL3) are the major regulators of plant transcriptional response to phosphate deficiency. Previously, we found that phl2phl3 double mutant is defective in shoot development, in which the expression of many SAM activity-related genes is altered. Furthermore, we found that PHL2 directly interacts with HAM family proteins. In this work, we would like to explore who PHL2/PHL3 and HAMs interact to regulate SAM activity. The results obtained from this work will provide insights in the molecular mechanism for how SAM activity is regulated.