The Role Of Pax1b In The Cardiovascular Development Of Zebrafish Embryos

Both Pax1and Pax9belong to Pax1/9subfamily of Paired box genefamily (PAX) which mainly participates in animal development andsclerotome differentiation. However, the role of Pax1in cardiovasculardevelopment and the precise mechanism remain unclear. In our study, wefound the expression patterns of zpax1b and zpax9were quite differentusing in situ hybridization and reverse-transcriptional PCR assay, andmicroinjection of morpholino (MO)-modified antisense oligonucleotidesagainst zpax1b induced pectoral fin bud and axial defects which could notbe phenocopied by pax9MO, and could not be rescued by either Pax1a orPax9overexpression，indicating zpax1b and zpax9had unique function inzebrafish embryo development. We further confirmed Loss-of-function ofzebrafish pax1b caused obvious malformation in heart and abnormal vesselsprouting: heart atrophy, disorder in intersegmental vessel (ISV), dificiencyin dorsal longitudinal anastomotic vessel (DLAV) and anastomotic vesselsamong ISV, suggesting pax1b played a vital role in zebrafishcardiovascular development. Furthermore, we found zpax1b knock downdecreased the expression of the triscription factors in relation tocardiovascular development including nkx2.5、 gata5and gata2in transcriptional level, increased the expression of p53, a tumor suppressor intranscriptional level, and overexpression of Pax1b decreased cell deathpotential on physiological stress. Together these evidences, we believedzpax1b participated in cardiovascular development, the regulation ofnkx2.5、gata2and gata5, cell apoptosis mediated by p53might be theimportant mechanism for cardiovascular defect caused by zpax1b knockdown. Further work is required to address the exact mechanism.