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This Week in PNAS: Jan 12, 2016

Editor's Note: Some of the articles described below are not yet available at the PNAS site, but they are scheduled to be posted some time this week.

Researchers in China have delved into the genomic incompatibilities that crop up in goldfish by common carp crosses in their study of polyploidy in animals, as they report in the Proceedings of the National Academy of Sciences. Using RNA sequencing, they uncovered a number of chimeric genes and mutations in gene orthologs in both diploid and tetraploid offspring of goldfish x common carp hybrids — the first two generations of hybrids are diploids, while subsequent ones are tetraploids. The diploid offspring, they note, show paternal-biased gene expression, though the tetraploids show maternal-biased expression. In addition, a portion of the chimeric and differentially expressed genes are involved in normal cell cycle activities and cancer-related pathways in 2nF1. These changes, the researchers report, appear to mostly be deleterious

Using a label-free quantitative proteomics-based approach, a University of Washington team of researchers has found that DAB2 regulates cardiac development and inhibits WNT/β-catenin signaling. The team examined the proteomes of human embryonic stem cells, cardiac progenitor cells, and cardiomyocytes during directed differentiation to find that DAB2 negatively regulates WNT/ β-catenin signaling. Further, DAB2 deletion in zebrafish leads to a decrease in the number of cardiomyocytes and to an increase in endogenous WNT/β-catenin signaling. This, they add, shows that proteomic studies of human stem cells can uncover new developmental regulators.

Finally, researchers in Tokyo report in PNAS that the long noncoding RNA UPAT promotes tumorigenesis in the colon by inhibiting UHRF1 degradation. The researchers performed RNA sequencing on the colon cancer cell line CCSC#P as well as on the CCSC#11 cell line, a subclone that shows decreased tumorigenicity. UPAT, they found, is downregulated in CCSC#11 and is needed for tumorigenicity in CCSC#P. It further, the researchers report, affects the ubiquitination and degradation of UHRF1, which itself helps up-regulate SCD1 and SPRY4, which aid colon tumor cells survive. This suggests that UPAT and UHRF1 could represent targets for colon cancer therapies, they add.