Skip to main content
Premium Trial:

Request an Annual Quote

This Week in Cell: Mar 8, 2017

An international team led by investigators in France describes a form of inborn error of innate immunity that could be reversed with antibodies targeting an immuno-stimulant produced by staph bacteria. The researchers did exome and targeted sequencing on a staph infection-prone child from a consanguineous family, narrowing in a mutation in TIRAP — a gene coding for a toll-like receptor (TLR) gene adaptor. They found the same TIRAP glitch in seven more members of the child's family and subsequently demonstrated that the mutation dialed down immune responses to TLRs. That problem was particularly pronounced in the original child, whose blood cells failed to react to TLRs tasked with recognizing staphylococcal lipoteichoic acid, the authors note, but could be largely reversed with a monoclonal antibody targeting lipoteichoic acid.

Researchers from Washington University and St. Jude Children's Research Hospital present evidence for enhanced CpG island hypermethylation as DNMT3A-mutated acute myeloid leukemia (AML) progresses. The team used whole-genome bisulfite sequencing to profile methylation in leukemic and non-leukemic cells from AML patients with or without a DNMT3A mutation that's typically linked to lower-than-usual methylation. The investigators saw signs that AML progression prompts a shift in DNMT3A activity, moving from diminished methylation in early stages of DNMT3A-mutated AML to a DNMT3A-dependent rise in methylation

A team from the UK explores the transcriptional consequences of ultraviolet irradiation exposure in human cells. Using a sequencing strategy designed to detect newly made RNA transcripts, radiolabeling, and other profiling approaches, the researchers saw sluggish transcript elongation, changes in gene activity, and a dip in long messenger RNA isoform production following UV exposure. In particular, irradiation prompted production of a regulatory, non-coding isoform from ASCC3, a gene that codes for a protein related to DNA damage response pathway. And, they note, that non-coding RNA was linked to transcriptional activity that was at odds with that associated with the ASCC3 protein itself.