Uracil processing by SMUG1 in the absence of UNG triggers homologous recombination and selectively kills BRCA1/2-deficient tumors.

Resistance to poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis) is the major obstacle to their effectiveness in the treatment of homologous recombination (HR)-deficient (HRD) tumors. Hence, developing alternative treatments for HRD tumors is critical. Here, we show that targeting the uracil excision pathway kills HRD tumors, including those with PARPi resistance.

SIN-3 acts in distinct complexes to regulate the germline transcriptional program in Caenorhabditis elegans.

The transcriptional co-regulator SIN3 influences gene expression through multiple interactions that include histone deacetylases. Haploinsufficiency and mutations in SIN3 are the underlying cause of Witteveen-Kolk syndrome and related intellectual disability and autism syndromes, emphasizing its key role in development. However, little is known about the diversity of its interactions and functions in developmental processes.

G protein-dependent signaling triggers a β-arrestin-scaffolded p70S6K/ rpS6 module that controls 5'TOP mRNA translation.

Many interaction partners of β-arrestins intervene in the control of mRNA translation. However, how β-arrestins regulate this cellular process has been poorly explored. In this study, we show that β-arrestins constitutively assemble a p70S6K/ribosomal protein S6 (rpS6) complex in HEK293 cells and in primary Sertoli cells of the testis.