Browse our latest Genetics and Genomics articles

Modulating the nutrient sensor TORC1 only in neurons in C. elegans is sufficient to regulate systemic longevity via inter-tissue signals that remodel mitochondria networks in non neuronal cells.

Regulatory evolution allows paralogs to escape from strucural pleiotropy.

Nematode hermaphroditism has co-evolved with a self-sperm sensing mechanism that protects hermaphrodites from the detrimental effects of mating with males.

Hermaphroditic Caenorhabditis elegans slow the onset of mating-induced death through self-sperm-regulated insulin-like gene expression, which regulates the activity of the IIS/FOXO pathway, mTOR signaling, and the TFEB/HLH-30 transcription factor.

Single-cell RNA-sequencing and germline substitutions provide novel insights into how testis is a hotspot for evolutionary innovation of genes, expression, and mutation at the single-cell level.

Young Caenorhabditis elegans hermaphrodites use their own sperm to protect against the negative consequences of mating.

A functional genetic variant, rs1690789, affects susceptibility to emphysema by altering TGFB2 expression in human lung fibroblasts.

Synonymous mutations can have highly variable fitness effects stemming from changes in transcription, some of which contribute to adaptation.

The role of an amino acid-dependent tRNA modification as a nutrient sensor and regulator of metabolic homeostasis has been discovered.

The transcription factor ztf-11 promotes neuronal differentiation by repressing other cell fates in the nematode worm C. elegans.