Richard Taylor

Richard Taylor

Research Associate


Local translation of mRNA underpins the development and function of?cell compartments located far from the soma, such as?neuronal axons and dendrites. To ensure proper local translation, local transcriptomic landscapes require tight regulation. Disruption of such regulation directly impacts on?local translation and subsequently the health and function of axons and dendrites.

My research is focused on better understanding localised RNA regulation in neurons; specifically?the role/s of intron retention. Introns are the 'non-coding' sequences classically spliced from pre-mRNAs following transcription in the nucleus. Intron-retaining transcripts are those in which one or multiple introns are not spliced.?Recently, we identified?that many intron-retaining transcripts are enriched in neuronal axons and dendrites compared to the soma. Very little is known about the role/s of such transcripts, and whether in this context?intronic sequence?encodes protein.

My work also studies how localised RNA?regulation is perturbed in neurodegeneration. SFPQ is an RNA-binding protein that predominantly functions as a splicing factor, but which also locates to axons and dendrites and regulates their?local?transcriptomes. SFPQ misregulation is a hallmark of Amyotrophic lateral sclerosis (ALS) regardless of the genetic cause of disease, suggesting that it may be a central player in pathogenesis.

Related News:

Novel ALS hallmark may trigger motor degeneration

New publication from the Houart lab

Selected publications:

Selected Publications

Taylor R, Houart C (2024) Optimized Primary Culture of Neuronal Populations for Subcellular Omics Applications. Methods Mol Biol 2707: 113-124
Nikolaou N, Gordon PM, Hamid F, Taylor R, Lloyd-Jones J, Makeyev EV, Houart C (2022) Cytoplasmic pool of U1 spliceosome protein SNRNP70 shapes the axonal transcriptome and regulates motor connectivity. Curr Biol

Taylor R, Hamid F, Fielding T, Gordon PM, Maloney M, Makeyev EV, Houart C (2022) Prematurely terminated intron-retaining mRNAs invade axons in SFPQ null-driven neurodegeneration and are a hallmark of ALS. Nat Commun 13: 6994