脊椎动物的造血过程受复杂而精密的信号网络所调控，其失衡可能导致严重发育异常。BCAS2是剪接复合体的一个成份，可能在真核细胞分化与发育中扮演重要角色，但对其研究尚少。前期工作中，我们应用 TALEN 技术构建了BCAS2敲除的斑马鱼模型，发现纯合缺失的幼鱼造血干细胞的迁移和分化异常，提示BCAS2可能在造血系统发育中发挥重要作用。本课题将在前期工作基础上，研究并确定BCAS2-/-斑马鱼造血干细胞发育和分化缺陷的具体阶段；研究BCAS2基因敲除是否通过Notch、cmyb/sdf1a信号通路影响造血干细胞发育或迁移, 是否通过调控细胞存活与增殖影响造血干细胞数量；通过转录组研究探索BCAS2影响造血干细胞发育新的分子信号网络并对其进行验证。本项目对于深入了解BCAS2在细胞分化和组织发育中的功能地位，和发现造血调控网络的新通路，均有重要意义。

The vertebrate hematopoiesis signal network is very complex and needs precise control, whose imbalance may lead to severe dysplasia. The fine regulation of hematopoiesis is not yet completely clear. BCAS2 is a component of spliceosome. It may play important roles in the differentiation and development of eukaryotic cells. In our preliminary work, we have applyed TALEN technology in constructing a BCAS2 knockout zebrafish model, in which significantly decreased juvenile blood cell number was identified, suggesting that BCAS2 may play an important role in the development of hematopoietic system. Based on the preliminary work, observation and analysis of the hematopoietic system development in different periods of the wild type and BCAS2-/- zebrafish will be carried out. And we will study effects of BCAS2 mutation on Notch and/or cmyb/sdf1 pathway, through wich the hematopoiesis process may be affected. We will also study whether BCAS2 regulates the hematopoitic stem cell number by affecting their survival and proliferation. Futhermore, we will investigate the transcriptome of zebrafish at different stages to uncover novel hematopoitic signalling pathways. This project will explore new mechanisms of BCAS2 in eukaryotic cells and will benefit the fully understanding about regulation network in hematopoiesis.