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. 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.