CONFERENCE COVERAGE SERIES
Brain Research Conference 2015: RNA Metabolism in Neurological Disease
Chicago, Illinois
15 – 16 October 2015
At the 10th Brain Research Conference: RNA Metabolism in Neurological Disease, a satellite of the Society for Neuroscience annual meeting, attendees learned about a parade of mice modeling different aspects of ALS and FTD that result from expansions in the C9ORF72 gene. Knockouts lose control of their immune systems, while transgenics overexpressing the repeat-heavy human gene ranged from normal to having movement and cognitive abnormalities. The results suggest the repeats cause toxicity, but scientists have plenty more to do to understand what the mice are telling them.
C9ORF72 Mice Point to Gain of Toxic Function in ALS, FTD
Phenotypes vary depending on the partial or full-length nature of the C9ORF72 transgene.
Does C9ORF72 Repeat RNA Promote Protein Phase Transitions?
The ALS-linked RNA may convert free-floating proteins to liquid phase droplets.
RNA Regulator Locked Out of Nucleus by C9ORF72 Repeats
The RNA-binding protein hnRNP A3 can help rid a cell of the repeat RNAs, but the RNAs interfere with its nuclear localization.
Listen Up, Gene Silencing Strikes a Chord at RNA Meeting
Scientists say treatments to muzzle faulty genes are making some headway.
Stressed Out: RNA-binding Protein Inhabits Granules in ALS, FTD
Meet RBM45. This RNA-binding protein and relatively new player in the ALS field associates with stress-induced structures in the cytoplasm and nucleus.
ALS Model Mice Roar Back When Human Transgene Silenced
Paralyzed mice recovered grip strength and balance when researchers turned off TDP-43.
Unexpected Polypeptides Pop Up in Huntington’s Disease
In a process known as repeat-associated non-ATG translation, neurons and glia make alanine, serine, cysteine, and leucine chains from the huntingtin gene.