The expression profiles of NCK and ABI genes after ESC
The expression profiles of NCK and ABI genes after ESC bacterial infection were determined. As shown in Fig. 1a, NCK1, ABI2a and ABI2b were significantly induced after ESC infection. While, ABI3a was significantly downregulated. Intestine was confirmed as a site of E. ictaluri entry by bacteriologic and microscopic methods (Baldwin and Newton, 1993). It has been reported that E. ictaluri crosses the intestinal mucosa of channel catfish in 15 min after oral inoculation (Baldwin and Newton, 1993). The upregulation of NCK1, ABI2a and ABI2b in intestine after ESC challenge indicated its involvement in the disease processes.
The most interesting findings were the observation of differential expression of the NCK and ABI genes between resistant and susceptible hybrid catfish (Fig. 1b). In general, the NCK and ABI genes, with exception of ABI3a gene and NCK1 gene, were expressed at higher levels in susceptible fish after infection than in control fish, but were expressed at lower levels in resistant fish than in the control fish. It appeared that the expression of most NCK and ABI genes were correlated with susceptibility. At present, we do not know why the genes were expressed at higher in susceptible fish and how the higher expression may be related to pathogenicity. However, NCK1 and NCK2 were reported to play an important role in linking cell surface receptor signaling to the actin-based cytoskeleton as a binding partner in other disease system such as infantile diarrhea (Gruenheid et al., 2001, Li et al., 2001, Todd, 1997). In humans, it was reported that the host protein NCK binds to a 12 residue amino BKT140 sequences of EPEC TIR in a phosphotyrosine-dependent manner and is recruited to EPEC to initiate actin remodeling and pedestal formation (Campellone et al., 2002, Gruenheid et al., 2001, Nieto-Pelegrin et al., 2014). NCK1, ABI1 and ABI2 were involved in regulation of actin dynamics for phagocytic cup formation, which is a crucial stage for phagocytosis (www.reactome.org). We do not know if this similar mechanism existed in the ESC situation, but this is certainly worthwhile of future studies. In our QTL mapping study, we mapped the ESC resistance QTL to a genomic region containing the NCK gene, which led us to speculate the involvement of catfish NCK in the pathogenesis of ESC (Zhou et al., 2017). The significant upregulation of NCK genes in catfish intestine and liver after ESC challenge supported the notion that NCK genes are involved in disease processes facilitating pathogenesis of the ESC bacteria.
Acknowledgement This project was supported by USDA National Institute of Food and Agriculture through a grant from Animal Disease Program (2015-67015-22975), and from Agriculture and Food Research Initiative Animal Genomics, Genetics and Breeding Program (2015-67015-22907). Tao Zhou is supported by a scholarship from the China Scholarship Council.
Introduction The first cell fate decision in mouse embryo takes place during 8- to 16- and 16- to 32-cell stage transition and is defined by a type of blastomere division. Divisions of blastomeres of 8- and 16-cell embryo can be classified as either conservative or differentiative depending on the later fate of two daughter cells. If division is conservative it generates two polar outer cells, which further will form the trophectoderm (TE). When a blastomere cleaves in a differentiative manner, it gives rise to one polar cell, which inherits the apical domain and remains on the embryo surface, and one apolar cell, which localizes inside the embryo and will form the inner cell mass (ICM) of the resulting blastocyst (Johnson and Ziomek, 1981). Thus, ICM cells are ultimately separated from TE cells as a result of two subsequent waves of differentiative divisions: during the transition from 8- to 16-cell stage (the first round of differentiative divisions) and from 16- to 32-cell stage (the second round of differentiative divisions). Additionally, in some embryos there is a third round of differentiative divisions at the 32- to 64-cell stage transition (Morris et al., 2010). Shortly before implantation the ICM cells differentiate into two sub-populations: the epiblast (EPI) – a source of cells for the future proper embryo and the primitive endoderm (PE), which contributes to the endoderm of the extraembryonic yolk sac.