Coordinated regulation of Rel expression by MAP3K4, CBP, and HDAC6 controls phenotypic switching.

Coordinated gene expression is required for phenotypic switching between epithelial and mesenchymal phenotypes during normal development and in disease states. Trophoblast stem (TS) cells undergo epithelial-mesenchymal transition (EMT) during implantation and placentation. Mechanisms coordinating gene expression during these processes are poorly understood.

GALNT3 Maintains the Epithelial State in Trophoblast Stem Cells.

O-GalNAc glycosylation is initiated in the Golgi by glycosyltransferases called GALNTs. Proteomic screens identified >600 O-GalNAc-modified proteins, but the biological relevance of these modifications has been difficult to determine. We have discovered a conserved function for GALNT3 in trophoblast stem (TS) cells, blastocyst trophectoderm, and human mammary epithelial cells (HMECs).

Innate immune response of channel catfish Ictalurus punctatus mannose-binding lectin to channel catfish virus (CCV).

The channel catfish virus (CCV) is a pathogenic herpesvirus that infects channel catfish Ictalurus punctatus in pond aquaculture in the southeastern USA. Mannose-binding lectin (MBL), an innate immune protein, could play an important role in the innate response of channel catfish by binding to CCV. Cell cultures of CCV were grown in channel catfish ovary cells (CCOC).

MAP3K4 Controls the Chromatin Modifier HDAC6 during Trophoblast Stem Cell Epithelial-to-Mesenchymal Transition.

The first epithelial-to-mesenchymal transition (EMT) occurs in trophoblast stem (TS) cells during implantation. Inactivation of the serine/threonine kinase MAP3K4 in TS cells (TS cells) induces an intermediate state of EMT, where cells retain stemness, lose epithelial markers, and gain mesenchymal characteristics. Investigation of relationships among MAP3K4 activity, stemness, and EMT in TS cells may reveal key regulators of EMT.