In a paper published online in advance this week, investigators at Stanford University School of Medicine and elsewhere show that miR-489 is "highly expressed in quiescent satellite cells and is quickly downregulated during satellite-cell activation." Further, the team found that miR-489 "functions as a regulator of satellite-cell quiescence, as it post-transcriptionally suppresses the oncogene Dek, the protein product of which localizes to the more differentiated daughter cell during asymmetric division of satellite cells and promotes the transient proliferative expansion of myogenic progenitors," and, as such, says its study provides evidence of an miRNA's active role in maintaining the quiescent state of an adult stem-cell population.
In another Nature advance online publication, researchers at the Massachusetts Institute of Technology, Washington University School of Medicine, and Baylor College of Medicine report their sequencing of the male-specific region of Y chromosome of the rhesus macaque, which they compared to the human MSY to address the question of "how many MSY genes were lost in the human lineage in the 25 million years that have followed its separation from the Old World monkey lineage." The team found that "MSY gene loss in the human lineage was limited to the youngest stratum, which comprises three percent of the human MSY," and that, similarly, "the rhesus MSY has not lost any older genes during the past 25 million years, despite its major structural differences to the human MSY," it reports. Our sister publication GenomeWeb Daily News has more on this study.
Elsewhere among this week's advance online papers is a study by researchers in the Netherlands and Sweden, who show that chromothripsis and neuritogenesis gene alterations frequently occur in high-risk neuroblastomas. In a whole-genome sequencing-based analysis of 87 neuroblastomas of all stages, the team reports few recurrent amino-acid-changing mutations, though several structural alterations that recurrently affected ODZ3, PTPRD and CSMD1. "In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma," the team writes. "Most tumors with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications."