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New research shows that the CoREST complex controls the acquisition of endocrine therapy resistance in estrogen receptor-positive breast cancers. Profiling data show that this resistance transition is accompanied by a functional retargeting of CoREST on chromatin in coordination with cJUN and SWI/SNF (cBAF).
The authors used massively parallel splicing assays and statistical learning to decode and predict the erroneous splicing choices made by disease-relevant mutant sequences, which annotates intronic variants potentially for clinical usage.
Here, the authors evaluate the performance of AlphaFold2 and its predicted structures on common structural biological applications, including missense variants, function and ligand binding site prediction, modeling of interactions and modeling of experimental structural data.
Cryo-EM structures of the AAA+ ClpAP•ClpS protease-adaptor complex show degron-like ClpS binding, coordinated by pore-1 loops from either the D1 or the D1 and D2 rings of ClpA. D1-pore-2-loop activity is critical for ClpS-assisted degradation.
Cryo-EM structures of simian immunodeficiency virus (SIV) envelope trimers with neutralizing antibodies reveal mechanisms—conserved throughout SIV evolution—of immune evasion through extended variable loops and glycan shielding, involving both N- and O-linked glycans.
Schmidpeter and colleagues showed that anionic lipids bind to pacemaker ion channels and increase their activity by acting like keys that unlock salt bridges at the channel gates.
The selection of polyadenylation signals defines 3′UTR length. The authors find that MYC alters the expression of factors that repress strong polyadenylation signals at the distal end of genes, boosting usage of suboptimal, proximal polyadenylation signals and promoting the translation of cell cycle-related genes.
Here, the structure of poly(UG) RNA reveals an unusual left-handed quadruplex, or ‘pUG fold’. The pUG fold marks RNAs as vectors for gene silencing in C. elegans by recruiting RNA-dependent RNA polymerase for siRNA synthesis.
Morey and colleagues identify a dual function of CoREST in regulating sensitivity and resistance to endocrine therapies in breast cancer. This work also provides a pre-clinical model for study of the conversion of luminal/ER+ to basal/ER− breast cancer.
Luan et al. find that CTCF shapes the transcriptional landscape in part by suppressing the initiation of upstream antisense transcription at hundreds of divergent gene promoters.