The ubiquitous NF-Y gene regulates the expression of different genes in various signaling pathways. However, the function of NF-Y in zebrafish heart development is largely unknown. Previously we identified a same group of cell cycle related gene cluster (CCRG) was downregulated in the embryonic hearts with impeded growth due to various stresses. The promoter regions of these CCRG genes shared a most common motif for NF-Y. Chromatin immunoprecipitation experiment demonstrated that the binding of NF-Y to its motif was real on the CCRG candidate gene promoters. Knockdown of embryonic NF-Y by morpholinos led to a small heart, mimicking the abnormal heart phenotype caused by other stresses. In parallel the expression of certain CCRG candidate genes was reduced in the NF-Y A morphant hearts exposed to malignant environments. Absence of NF-Y A also led to undermine cardiomyocyte proliferation and hence less total number of caridomyocytes per heart. Trans-AM Elisa experiment also found that in the presence of the stresses such as TCDD and TNNT2 MO, the binding capacity of NF-Y A subunit to its core motif was reduced. We conclude that NF-Y sustains proper cardiomyocyte proliferation in the heart, thus it plays a positive role in promoting early zebrafish heart growth.
Keywords: NF-Y; cardiomyocyte proliferation; development; embryonic heart; zebrafish.
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