Bves is widely observed in the cell junction of the skin, epicardium, intestine, and cornea of both developmental embryos
and mature adults. However, it is not clear how Bves confers its role in intercellular adhesion. Here, we identified the zebrafish
bves (zBves) and found that the epidermal barrier function could be disrupted after knockdown of Bves, and these zBves morphants
were sensitive to osmotic stress. A loss of zBves would affect the PAR junctional complex identified by the rescue experiment
with tjp-2/ZO-2 or the PAR complex (par-3, par-6, and prkci/aPKC) mRNAs, in which the survival rate of embryos increased 11%,
24%, 25%, and 28%, respectively, after injection with junctional components; the tjp-2 and aPKC mRNA-rescued embryos also
had 24% and 45% decreases in the defective rate. Immunofluorescent studies demonstrated that the aggregation of aPKC around
the cell junctions was disintegrated in zBves morphants. However, the expression and assembly of zBves was not influenced.
by aPKC-MO, These results indicate that a loss of zBves affects the proteins involved in the pathway of the PAR junctional
complex, especially aPKC and both aPKC and Bves are indispensable to claudin expression.