Zheng, X., Yang, S., Han, Y., Zhao, X., Zhao, L., Tian, T., Tong, J., Xu, P., Xiong, C., and Meng, A. (2012) Loss of zygotic NUP107 protein causes missing of pharyngeal skeleton and other tissue defects with impaired nuclear pore function in zebrafish embryos. The Journal of biological chemistry. 287(45):38254-38264.
The Nup107-160 multiprotein subcomplex is essential for the assembly of nuclear pore complexes. The developmental functions
of individual constituents of this subcomplex in vertebrates remain elusive. In particular, it is unknown whether Nup107 plays
an important role in development of vertebrate embryos. Zebrafish nup107 is maternally expressed and its zygotic expression
becomes prominent in the head region and the intestine from 24 hours postfertilization (hpf) onward. In this study, we generate
a zebrafish mutant line, nup107tsu068Gt, in which the nup107 locus is disrupted by an insertion of Tol2 transposon element
in the first intron and as a result it fails to produce normal transcripts. Homozygous nup107tsu068Gt mutant embryos exhibit
tissue-specific defects after 3 days postfertilization (dpf), including loss of the pharyngeal skeletons, degeneration of
the intestine, absence of the swim bladder, and smaller eyes. These mutants die at 5-6 days. Extensive apoptosis occurs in
the affected tissues, which is partially dependent on p53 apoptotic pathways. In cells of the defective tissues, FG-repeat
nucleoporins are disturbed and nuclear pore number is reduced, leading to impaired translocation of mRNAs from the nucleus
to the cytoplasm. Our findings shed new light on developmental function of Nup107 in vertebrates.