In csw mutant embryos, HB does not retract from the pole, but remains as a terminal cap. This altered pattern of hb expression is like that observed in huckebein mutant embryos where hb continues to be expressed at the pole due to lack of the Huckebein repressing activity. As in hkb mutants, csw mutant embryos exhibit a reduction in fkh posteriorly. In csw mutant embryos as in hkb mutants, the seventh ftz stripe, while present, is expanded posteriorly. Taken together, these data suggest that maternally provided csw positively affects the activity of tailless , as well as further downstream genes of the terminal system.
Embryos null for csw , with a hypomorphic allele of raf show no tll activity.
Protein Interactions Tyrosines 630 and 918 are the major sites of TOR autophosphorylation. Mutation of tyrosine 630, a site required for association with and tyrosine phosphorylation of the tyrosine phosphatase Corkscrew, decreases the efficiency of TOR signaling. In contrast, mutation of Y918, a site capable of binding mammalian rasGAP and PLC-gamma1, increases TOR signaling. When receptors contain mutations in both sites, TOR signaling is restored to wild-type levels. CSW becomes tyrosine phosphorylated as a direct result of TOR ligand induced activation.