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Coordinated hormonal interactions in response to feeding and fasting regulate glucose homeostasis. Here the authors report that Activin B, expressed in the liver sinusoidal endothelial cells, is involved in glucose homeostasis by regulating hepatic FGF21 production and glucagon sensitivity and can be inhibited by adipocyte-derived FSTL3 during obesity.

Metabolic, immune and endocrine systems undergo seasonal changes in animals. Here the authors report the seasonal transcriptome of 80 tissues collected over 1 year from male and female rhesus macaques as well as sex differences in seasonally oscillating genes.

Analysis of the blood DNA virome in patients with COVID-19 and autoimmune disease associates endogenous HHV-6 (eHHV-6) and high anellovirus load with increased disease risk, most notably for systemic lupus erythematosus. eHHV-6 carriers show a distinct immune response.

A genome-wide association study highlights a variant in DOCK2, which is common in East Asian populations but rare in Europeans, as a host genetic risk factor for severe COVID-19.

It is difficult to investigate the chemical properties of superheavy elements, which are only available an atom at a time and rapidly decay. A co-precipitation method with samarium has now been developed that suggests rutherfordium would form hydroxide precipitates—but not ammine ones—if it were possible to perform these experiments on macroscopic quantities.

Ito et al. present CoVFit, an AI model that predicts variant fitness (transmissibility) from spike protein sequences alone. They further demonstrate its utility in forecasting viral evolution via single amino acid mutations.

Brain cells that die after stroke release intracellular proteins into their environment. Akihiko Yoshimura and his colleagues demonstrate that peroxiredoxin proteins released from dying cells induce inflammatory cytokine expression and drive brain damage after stroke.

XBB.1.5 of SARS-CoV-2 is a descendant of XBB.1 and has mutations in spike and ORF8, making it more infectious to humans. Here, the authors examined in detail the differences in virological properties of the two variants.

Transfer of NR4A-deficient T cells expressing chimeric antigen receptors is shown to reduce tumour burden and increase survival by shifting T cell transcriptional programs away from exhaustion and towards increased effector function.

Inflammatory cells invade the brain after stroke, but their role in disease has been unclear. Now, Akihiko Yoshimura and colleagues report that a particular population of T cells that express the inflammatory cytokine IL-17 plays a key role in stroke progression: depletion of these cells—even as late as 1 day after stroke—can alleviate brain injury in mice pages 844–846).

The P681R mutation in the spike protein renders the Delta variant more pathogenic than prototypic SARS-CoV-2 in infected hamsters, and facilitates spike protein cleavage and enhances viral fusogenicity.

Tumour-specific T cells can be expandedin vitroand adoptively transferred for therapy, but this strategy is limited by induction of short-lived T cell populations. Here the authors activate Notch signalling in cultured mouse or human T cells, resulting in the production of a long-lived stem cell memory T cell population that can fight tumours in mice.

The regulation of meiotic prophase progression varies between males and females. This study reveals the involvement of an atypical heat shock transcription factor HSF5 in gene expression during male meiotic prophase and highlights the involved gene regulatory mechanism.

These authors contributed equally to this work:

Short tandem repeat mutations in a primate Alu element on chromosome 15q cause activation of a thyroid-specific enhancer, upregulating MIR7-2/MIR1179. This results in defective thyroid proliferation and thyrotropin resistance.

JN.1 lineage is a globally dominant variant of SARS-CoV-2. Here, the authors examine structural insights into the BA.2.86 and JN.1 spike dynamics to help understand the mechanisms underlying SARS-CoV-2 infection and its neutralizing-antibody evasion.

The gut is populated by a myriad of microorganisms and how the immune system tolerates their presence is of great interest. Here, by studying colon morphology in multiple knockout mice, the authors demonstrate a potential role for prostaglandin E2 and SOCS1 in mediating immune tolerance.

This paper examines the changes in gene expression during the first exposure to a long day (such as those found in spring) in Japanese quails and find that two waves of genes are induced as part of the photoperiodic response. This paper also identifies thyrotrophin expression in the pars tuberalis as a critical event in triggering this photoperiodic response.

Relapse is a limitation for the efficacy of the anaplastic lymphoma kinase (ALK)-inhibitor alectinib in ALK-rearranged lung cancer. Here, the authors show that YAP1 activation upon alectinib treatment leads to therapy resistance and that inhibiting both YAP1 and ALK leads to longer tumor remission in mice.

In vitro studies in human cell lines and in vivo studies in a hamster model show that the SARS-CoV-2 Omicron variant is less pathogenic than both the Delta variant and an ancestral strain of SARS-CoV-2.

In a mouse model of ischaemic stroke, regulatory T cells infiltrate the injured brain in response to the chemokines CCL1 and CCL20 and suppress excessive astrogliosis via the production of amphiregulin.

The fabrication of transistors using vertical, six-sided core–multishell indium gallium arsenide nanowires with an all-surrounding gate on a silicon substrate combines the advantages of a three-dimensional gate architecture with the high electron mobility of the III–V nanowires, drastically enhancing the on-state current and transconductance.

Regulatory T cells are characterized by the expression of Foxp3, however, how the expression of this protein is controlled is unclear. Here, the authors show that the nuclear orphan receptor, Nr4a2, is a transcriptional activator of Foxp3, and suggest that it is required for the function of regulatory T cells.

Activation of inflammasome contributes to several pathologies. Here, the authors show that Bruton’s tyrosine kinase is essential for NLRP3 inflammasome activation, and that blocking it with the FDA-approved inhibitor ibrutinib limits tissue damage in a mouse model of ischaemic stroke.

Sekiya and colleagues demonstrate that the Nr4a nuclear receptors, which are encoded by immediate-early genes upregulated by TCR stimulation in thymocytes, have an essential role in regulatory T cell development.

XBB is the first recombinant, globally dominant variant of SARS-CoV-2. Here, the authors examine the variant’s origins and virological properties, showing it is the first example of SARS-CoV-2 improving its fitness through recombination.

Recent Omicron SARS-CoV-2 subvariants independently acquire 5 key Spike mutations. Here, the authors evaluate the evolutionary importance of the 5 mutations and characterize the virological properties of variant BQ.1.1 harboring all 5 mutations.

Personal information such as genetic sex, ancestry and clinically relevant genetic variants can be recovered from human reads present in faecal metagenomic sequencing data.

This study identifies TTTCA- and TTTTA-repeat expansions in benign adult familial myoclonic epilepsy. Cortical neurons from affected people exhibit RNA foci containing these expanded repeats, suggesting RNA toxicity as the mechanism underlying disease pathogenesis.