Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
X-chromosome inactivation studies have revealed striking species specificities in terms of the players, kinetics and mechanisms. Transcriptomic profiling of human pre‐implantation development and germ cell differentiation suggests a peculiar dosage compensation mechanism with yet undefined contributions from XIST and XACT lncRNAs.
Haltalli et al. show that Plasmodium berghei infection induces interferon release, and affects haematopoietic stem cell proliferation and function, as well as osteoblasts and vascular integrity, in the bone marrow niche.
Espanola et al. show in zebrafish that Supt16h, a component of the FACT complex, regulates HSC development through an increase of p53, which promotes expression of phc1, a transcriptional repressor of Notch.
Nguyen et al. show in mouse testes that germ cells are eliminated via apoptosis if they fail to differentiate properly due to errors in epigenetic reprogramming, a process that improves gamete quality.
Chitiashvili et al. report that X-chromosome dosage compensation is achieved via X-chromosome dampening in human female primordial germ cells (hPGCs) and reveal that the lncRNA XACT is a hPGC marker.
Luo et al. report that heat stress activates YAP to launch the heat shock transcriptome through inducing dephosphorylation and degradation of LATS independent of the upstream kinases MST and MAP4Ks.
Lamm et al. report that replication stress activates mTOR through ATR to induce nuclear actin polymerization, facilitating the recovery from replication stress.