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.
Kramer, Prakash et al. share genome-wide CRISPR screens for factors that alter the levels of two dual-genome-encoded Complex IV subunits, COX1 and COX4. They identify PREPL and NME6 as genes that connect mitochondrial metabolism to mtDNA expression.
Zhang et al. report curved adhesions, which are integrin-based adhesions formed in response to membrane curvatures that can be imposed by the overlying extracellular matrix fibre geometry.
In many species, maternally deposited Piwi-interacting RNAs (piRNAs) deliver intergenerational epigenetic information to protect progeny from transposon expansion or invasion. However, Y-chromosome-encoded piRNAs cannot be passed from mothers to male offspring, yet mothers use autosomally encoded piRNAs to allow sons to utilize their Y chromosome to protect against ‘selfish’ elements.
In this issue, Jason Shapiro, Hsiang-Chun (Jimmy) Chang and colleagues identify a conserved role for the iron-binding histone demethylase KDM3B in sensing iron levels and regulating mTORC1 through transcriptional repression of key components of the mTORC1 pathway. In this Q&A, we discuss this manuscript’s findings and publishing journey with first authors Jason Shapiro and Jimmy Chang and corresponding author Hossein Ardehali. Hossein is currently the director of the Center for Molecular Cardiology at the Feinberg School of Medicine at Northwestern University in Chicago; Jason is an MD candidate graduating in 2024 at the Feinberg School of Medicine; and Jimmy is a resident physician in the Department of Pediatrics at the Baylor College of Medicine in Houston.
Shapiro, Chang, et al. identify a conserved role for the iron-binding histone demethylase KDM3B in sensing iron levels and regulating mTORC1 through transcriptional repression of key mTORC1 pathway components.
Bernabé-Rubio et al. report that dedifferentiation of Gata6+ epidermal cells occurs during wound healing or mechanical expansion of the epidermis through a Myc-dependent process that resembles reversal of differentiation.
Venkei et al. show that Y-linked Su(Ste) piRNAs are produced via 5′-to-3′ phased-biogenesis initiated by maternally deposited 1360/Hoppel-derived piRNAs, leading to silencing of Ste in the male germline.
Huang, Li, An, Yang, Cui et al. perform a single-cell multi-omics analysis of human spermatogenesis and identify a DNA demethylation event upon meiosis initiation, which is associated with meiotic recombination.
The molecular program of human germline commitment remains largely unknown. A new study delineates the multifaceted functions of DMRT1 in human germline development, particularly in the transition from early to late primordial germ cells.
Irie, Lee et al. report a role for DMRT1 in human germline development and show that induction of DMRT1 in primordial germ cell-like cells triggers germline commitment, but suppresses pluripotency genes, thus promoting the onset of gametogenesis.
Shirin Bahmanyar is an associate professor of molecular, cellular & developmental biology at Yale University, CT, USA. Shirin’s lab studies the organization of the endoplasmic reticulum (ER) and nuclear envelope, their dynamics throughout the cell cycle, and their relationship to lipid metabolism. We reached out to Shirin and were delighted to hear her thoughts on open questions in this field and to learn more about her research background and interests.
RNA modifications have emerged as key gene regulators. A new study shows that increased levels of reactive oxygen species in cancer induce widespread, sequence-specific modifications of guanines in the seed regions of microRNAs, altering the targets of those miRNAs and influencing tumorigenesis.
Embryonic diapause in development and paused pluripotency in embryonic stem cells result in a state of hypotranscription through mechanisms that remain unclear. A new study dissects the role of METTL3-deposited global m6A RNA methylation in mediating this transcriptional dormancy.
Collignon et al. report that Mettl3-mediated m6A RNA methylation promotes developmental pausing in embryonic stem cells and blastocysts by establishing transcriptional dormancy.
