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Transcriptional activator-like effectors (TALEs) have emerged as powerful tools for genome editing. A recent study published by Cell Research reports that fusion of thioredoxin to TALEs unlocks their full potential in live-cell imaging to accurately analyze genome instability, telomere attrition and epigenetic alterations that are hallmarks of aging.
EGF, a well-studied mitogen for cancer cells, is revealed to induce an E3 ubiquitin ligase adaptor SPSB1, which recruits the Elongin B/C-Collin complex to trigger ubiquitylation of the negative splicing regulator hnRNP A1. This event is synergized with EGF-activated SR proteins to alter alternative splicing of a key small GTPase Rac1 to enhance cell migration, highlighting converging EGF signals on both negative and positive splicing regulators to jointly promote a key cancer pathway.
In a recent Nature paper, Heintz et al. identify a splicing factor (SFA-1) that is crucial for the longevity conferred by dietary restriction and the TORC1 pathway modulation in C. elegans.
The molecular mechanisms governing self-renewal and differentiation of the mammary epithelium are incompletely defined; a better understanding of the events implicated in the specification and expansion of luminal progenitors is of particular importance as many breast cancers originate from their transformation. Britschgi et al. found that, in addition to phosphorylating and inactivating YAP, LATS functions as a scaffold to facilitate estrogen receptor-α ubiquitylation by the E3 ligase CRL4DCAF1 and consequently suppresses luminal progenitor specification and expansion.
