ME31B is a general repressor of gene expression in the Drosophila early embryo, repressing translation before the maternal-to-zygotic transition and stimulating mRNA decay after activation of the zygotic genome.

New analyses shift the view that some forms of amyotrophic lateral sclerosis and frontotemporal dementia are due to defects in a single RNA-binding protein.

The kinase that controls maternal mRNA translation is regulated by phosphorylation of its activating subunit to restrict kinase activity to the developmental window between meiosis completion and early embryogenesis.

The threonine kinase controls maternal mRNA translation phosphorylate components of the translational machinery, including translational repressors, which appear to inactivate to promote the oocyte-to-embryo transition.

Idiopathic patients along a complex motor neuron disease-dementia spectrum exhibit mRNA splicing changes that are due to multi-protein insolubility.

Several support cell populations balance progenitor maintenance with differentiation in zebrafish lateral line sensory organs.

The C9orf72 expansion binds and sequesters the splicing factor hnRNP H leading to insoluble G-quadruplex aggregates that functionally reduce hnRNP H, thereby producing splicing defects.

The retarding effect of a ribosome-bound internal ribosome entry site on eukaryotic protein synthesis is largely overcome following translocation of tripeptidyl-tRNA.

A Internal Ribosomal Entry Site RNA has been visualised by high resolution cryoEM, trapped in the ribosome in an intermediate state of translocation.

The MEG (maternal-effect germline defective) proteins, MEG-1, 2, 3 and 4, regulate RNA granule dynamics in vivo.