How epithelial cell fates become specified is poorly understood. We have previously shown that the putative zinc-finger transcription factor LIN-26 is required for the differentiation of ectodermal and mesodermal epithelial cells in Caenorhabditis elegans . To further investigate the role of
lin-26 , we analysed the consequences of ectopic
lin-26 expression under a heat-shock promoter. Ectopic LIN-26 expression at a specific time-window, during early gastrulation, transforms most blastomeres into epithelial-like cells. Specifically, overexpression of LIN-26 induced an overexpression of the three following epithelial markers: i) the apical junction protein JAM-1 which is recognised by the MH27 antibody, ii) DLG-1, a protein of the MAGUK family, which is essential for the assembly of JAM-1 at junctions, and iii) CHE-14, a transmembrane protein involved in apical vesicle trafficking. Furthermore, ultrastructural studies revealed that ectopic LIN-26 expression induced the formation of apical-like junctions both in external and internal cells. However, ectopic
lin-26 expression did not confer any tissue-specific cell fate, such as the hypodermal cell fate, as evidenced from the observation that several hypodermal-specific genes were not induced. Conversely, we have shown that in
lin-26 mutants, JAM-1 and CHE-14 patterns display some polarity defects, and that about half of the apical junctions were abnormal in the hypodermis, consistent with a role of
lin-26 in epithelial differentiation. The persistent expression of
jam-1 and
che-14 in
lin-26 null mutants suggests that these two genes are controlled by parallel pathways including
lin-26 and presumably by genes that has been shown to control ectodermal differentiation, such as GATA factors
elt-1 and
elt-3 . Finally, we conclude that
lin-26 can induce epithelial differentiation without conferring any tissue specificity and that epitheliogenesis is not a default pathway in C. elegans .