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Meiosis is key to sexual reproduction and genetic diversity. Here, we show that the Arabidopsis cyclin‐dependent kinase Cdk1/Cdk2 homolog CDKA;1 is an important regulator of meiosis needed for several aspects of meiosis such as chromosome synapsis. We identify the chromosome axis protein ASYNAPTIC 1 (ASY1), the Arabidopsis homolog of Hop1 (homolog pairing 1), essential for synaptonemal complex formation, as a target of CDKA;1. The phosphorylation of ASY1 is required for its recruitment to the chromosome axis via ASYNAPTIC 3 (ASY3), the Arabidopsis reductional division 1 (Red1) homolog, counteracting the disassembly activity of the AAA + ATPase PACHYTENE CHECKPOINT 2 (PCH2). Furthermore, we have identified the closure motif in ASY1, typical for HORMA domain proteins, and provide evidence that the phosphorylation of ASY1 regulates the putative self‐polymerization of ASY1 along the chromosome axis. Hence, the phosphorylation of ASY1 by CDKA;1 appears to be a two‐pronged mechanism to initiate chromosome axis formation in meiosis., Phosphorylation of the HORMA domain protein ASY1 by the central cell cycle kinase promotes its recruitment onto meiotic chromosomes both via protein interactions and by countering disassembly ATPase PCH2.

Summary Understanding the mechanisms of cancer initiation will help to prevent and manage the disease. At present, the role of the breast microenvironment in transformation remains unknown. As BMP2 and BMP4 are important regulators of stem cells and their niches in many tissues, we investigated their function in early phases of breast cancer. BMP2 production by tumor microenvironment appeared to be specifically upregulated in luminal tumors. Chronic exposure of immature human mammary epithelial cells to high BMP2 levels initiated transformation toward a luminal tumor-like phenotype, mediated by the receptor BMPR1B. Under physiological conditions, BMP2 controlled the maintenance and differentiation of early luminal progenitors, while BMP4 acted on stem cells/myoepithelial progenitors. Our data also suggest that microenvironment-induced overexpression of BMP2 may result from carcinogenic exposure. We reveal a role for BMP2 and the breast microenvironment in the initiation of stem cell transformation, thus providing insight into the etiology of luminal breast cancer., Graphical Abstract, Highlights • High BMP2 levels are provided by endothelial and stroma cells in luminal tumors • Chronic exposure to high BMP2 levels initiate mammary epithelial transformation • Luminal tumors likely arise from an amplified BMP2/BMPR1B-mediated normal response • Radiation and bisphenols perturbed BMP2 production by the mammary niche stroma, Carcinogens alter stromal cells, increasing local concentrations of BMP2 as specifically measured in human breast luminal tumors. Chronic exposure of immature mammary epithelial cells to high BMP2 levels initiated transformation toward a luminal tumor-like phenotype through the receptor BMPR1B. Maguer-Satta and colleagues show that the stem cell microenvironment could therefore represent a driving force to promote transformation and dictate the ultimate breast tumor subtype.

Germ cells on demand Unlike animals, plants do not set aside a germline. Instead, germ cells are developed on demand from somatic lineages. Zhao et al. examined the regulatory pathways that manage the transition from somatic to germ cell development in the small plant Arabidopsis (see the Perspective by Vielle-Calzada). The transcription factor WUSCHEL (WUS) was needed early on for development of ovules. Soon after, a trio of inhibitors that work through a cyclin-dependent kinase allowed a transcriptional repressor to down-regulate WUS. This opened the door to meiosis, while restricting the number of reproductive units per seed to one. Science , this issue p. eaaf6532 ; see also p. 378

Upon DNA damage, cyclin‐dependent kinases (CDKs) are typically inhibited to block cell division. In many organisms, however, it has been found that CDK activity is required for DNA repair, especially for homology‐dependent repair (HR), resulting in the conundrum how mitotic arrest and repair can be reconciled. Here, we show that Arabidopsis thaliana solves this dilemma by a division of labor strategy. We identify the plant‐specific B1‐type CDKs (CDKB1s) and the class of B1‐type cyclins (CYCB1s) as major regulators of HR in plants. We find that RADIATION SENSITIVE 51 (RAD51), a core mediator of HR, is a substrate of CDKB1‐CYCB1 complexes. Conversely, mutants in CDKB1 and CYCB1 fail to recruit RAD51 to damaged DNA. CYCB1;1 is specifically activated after DNA damage and we show that this activation is directly controlled by SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a transcription factor that acts similarly to p53 in animals. Thus, while the major mitotic cell‐cycle activity is blocked after DNA damage, CDKB1‐CYCB1 complexes are specifically activated to mediate HR.