Mutations in
tcl-2 cause defects in the specification of the fates of the descendants of the TL and TR blast cells, whose polarity is regulated by
lin-44/Wnt and
lin-17/frizzled, during Caenorhabditis elegans development. In wild-type animals, POP-1/TCF/LEF, is asymmetrically distributed to the T cell daughters, resulting in a higher level of POP-1 in the nucleus of the anterior daughter. The POP-1 asymmetric distribution is controlled by
lin-44 and
lin-17. However, in
tcl-2 mutants, POP-1 is equally distributed to T cell daughters as is observed in
lin-17 mutants, indicating that, like
lin-17,
tcl-2 functions upstream of pop-L In addition,
tcl-2 mutations cause defects in the development of the gonad and the specification of fate of the posterior daughter of the P12 cell, both of which are controlled by the Wnt pathway. Double mutant analyses indicate that
tcl-2 can act synergistically with the Wnt pathway to control gonad development as well as P12 descendant cell fate specification.
tcl-2 encodes a novel protein. A functional
tcl-2::gfp construct was weakly expressed in the nuclei of the T cell and its descendants. Our results suggest that
tcl-2 functions with Wnt pathways to control T cell fate specification, gonad development, and P12 cell fate