造血干细胞（HSC）发育缺陷会引起各种血细胞或血管发育障碍，并与很多血液系统疾病密切相关。胚胎期HSC的迁移是HSC正确发育的必经阶段，然而人们对胚胎发育期HSC迁移的机制知之甚少。本项目将以斑马鱼为模型，以前期工作中发现的cMyb对胚胎期HSC的迁移调控为研究基础，拟继续探讨cMyb调控胚胎期HSC迁移的细胞及分子机理，计划围绕以下问题进行研究：cMyb基因参与调控胚胎期HSC迁移的细胞学机理；cMyb基因参与调控胚胎期HSC迁移的下游信号途径；胚胎期HSC迁移调控中cMyb与Cd41是否有关；以及cMyb在调控非HSC细胞迁移方面的功能。本研究将逐步阐明胚胎期HSC的迁移机制，为人类相关疾病的发病机理的研究提供理论依据，并对相关的药物筛选及疾病诊断治疗等方面提供模型支持。

The defects of hematopoietic stem cell (HSC) development can cause kinds of blood system defects, and associates with many human blood diseases. The HSC migration is a key step for HSC pool establishment. The mechanism of HSC migration during embryonic stage is unclear. Our group reported that the transcription factor cMyb is essential for HSC migration in zebrafish. In this proposal, we are focus on the unknown questions for cMyb regulated HSC migration, including unveiling the cellular basis of cmyb defect HSC, searching downstream genes of cMyb, verifying the co-factor of cMyb, and confirming whether cMyb is involved in other non-HSC migration. Our research will unveil more new mechanisms of embryonic HSC migration and will help us to understand the mechanism and provide more molecular evidences for related human diseases.