Guo M, Bier E, Jan L Y, Jan Y N
Howard Hughes Medical Institute, Department of Physiology, University of California at San Francisco 94143, USA.
Neuron. 1995 May;14(5):913-25. doi: 10.1016/0896-6273(95)90330-5.
Asymmetric cell divisions allow a sensory organ precursor (SOP) cell to generate a neuron and its support cells in the Drosophila PNS. We demonstrate a role of tramtrack (ttk), previously identified as a zinc finger-containing putative transcription factor, in the determination of different daughter cell fates. Both loss of function and overexpression of ttk affect the fates of the SOP progeny. Whereas loss of ttk function transforms support cells to neurons, ttk overexpression results in the reverse transformation. ttk is expressed in support cells but not in neurons. It has been shown that numb, a membrane-associated protein asymmetrically distributed during the SOP division, confers different daughter cell fates. Loss of ttk or numb function results in reciprocal cell fate transformation. Epistatic studies suggest that ttk acts downstream of numb. We propose that ttk executes the command dictated by asymmetrically localized numb to specify distinct daughter cell fates during multiple asymmetric divisions.
不对称细胞分裂使感觉器官前体细胞（SOP）在果蝇外周神经系统中产生一个神经元及其支持细胞。我们证明了先前被鉴定为含锌指的假定转录因子的tramtrack（ttk）在确定不同子细胞命运中的作用。ttk的功能丧失和过表达都会影响SOP后代的命运。ttk功能丧失会将支持细胞转变为神经元，而ttk过表达则导致相反的转变。ttk在支持细胞中表达，但在神经元中不表达。已经表明，麻木蛋白是一种在SOP分裂期间不对称分布的膜相关蛋白，它赋予不同的子细胞命运。ttk或麻木蛋白功能的丧失会导致相互的细胞命运转变。上位性研究表明ttk在麻木蛋白的下游起作用。我们提出，ttk执行由不对称定位的麻木蛋白所决定的指令，以在多个不对称分裂过程中指定不同的子细胞命运。
