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In marine bacteria, carotenoids enhance rhodopsin function by acting as light-harvesting antennae and photocycle-accelerating pigments, a dual mechanism that enhances light energy capture and expands the known strategies of microbial phototrophy.

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 single-cell multiomic immune cell atlas from 235 Japanese, including patients with COVID-19 and healthy individuals, linked with host genetics including germline and somatic mutation, plasma proteomics and metagenomics data reveals that immune cells are dynamically regulated in a cell state-dependent manner.

Genetic mechanisms influencing COVID-19 susceptibility are not well understood. Here, the authors analyzed whole blood RNA-seq data of 465 Japanese individuals with COVID-19, highlighting thousands of fine-mapped variants affecting expression and splicing of genes, as well as the presence of COVID-19 severity-interaction eQTLs.

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.

Ikeda et al. report that HLA-DRB1 can serve as a leukemia-specific target for CAR T or natural killer cell-based therapy in patients with AML after allogeneic hematopoietic stem cell transplantation.

Uncultured open-ocean Asgard archaea can harvest light energy using rhodopsins and diverse hydroxylated carotenoid antennas.

A global network of researchers was formed to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity; this paper reports 13 genome-wide significant loci and potentially actionable mechanisms in response to infection.

Peripheral blood mononuclear cells from 73 Japanese patients with coronavirus disease 2019 (COVID-19) and 75 healthy controls were analyzed using single-cell transcriptomics. Combining these data with genotyping data highlights the interplay between host genetics and the immune response in modulating disease severity.

Somatic mutations in ASXL1 lead to clonal hematopoiesis, and Sato et al. elucidate the molecular mechanisms by which mutated ASXL1 in hematopoietic cells drives atherosclerosis in mice.

Here the authors show that Fam102a positively regulates osteoblast differentiation by promoting Osterix expression via Runx2 and Rbpjl. Loss of Fam102a or mutation of Rbpjl causes osteopenia, highlighting the critical role of the Fam102a-Rbpjl axis in bone remodeling.

Tanaka and colleagues perform a comprehensive multi-omic characterization of peritoneal metastasis of gastric cancer to define molecular subtypes and actionable therapeutic targets.

Light energy transfer from abundant hydroxylated carotenoids to the retinal moiety of widespread light-driven proton pumps is detected.

The structure of human prostaglandin E receptor EP4 in complex with antagonist ONO-AE3-208 and a functional antibody reveals a ligand-binding site at the interface of the lipid bilayer that is unique among GPCRs.

Uterine adenomyosis often co-occurs with endometriosis or leiomyoma, but little is known about its molecular underpinnings. Here, the authors show that KRAS mutations are frequent in this disease, which might reduce sensitivity to progestin treatment via epigenetic silencing of the progesterone receptor.

Mammalian genomes are scattered with repetitive sequences, but their biology remains largely elusive. Here, the authors show that transcription can initiate from short tandem repetitive sequences, and that genetic variants linked to human diseases are preferentially found at repeats with high transcription initiation level.

ASXL1 mutations are frequently found in age-related clonal haemaotopoiesis (CH), but how they drive CH is unclear. Here the authors show that expression of C-terminal truncated ASXL1 in haematopoietic stem cells (HSCs) leads to Akt de-ubiquitination, activated Akt/mTOR signaling, and aberrant HSC proliferation.

A liver–brain–gut neural circuit responds to the gut microenvironment and regulates the activity of peripheral regulatory T cells in the colon by controlling intestinal antigen-presenting cells in a muscarinic signalling-dependent manner.

ASXL1 gene is often mutated in myeloid malignancies. Here, the authors show that mutant ASXL1 and BAP1 are in a positive feedback loop such that BAP1 induces monoubiquitination of mutant ASXL1, which in turn enhances BAP1 activity to potentiate myeloid transformation via HOXA clusters and IRF8.

Wide-bandgap transistors with room-temperature hole mobility of 680 cm² V⁻¹ s⁻¹ can be created without surface doping using hydrogen-terminated diamond/hexagonal boron nitride heterostructures.

Very little is known about how chromatin-modifying enzymes are regulated in response to signalling cascades. A jmjc demethylase, PHF2, is found to be activated by PKA-mediated phosphorylation, which promotes its association with the DNA-binding protein ARID5B. PHF2 then induces demethylation of ARID5B, and the PHF2–ARID5B complex modifies histone at its target promoters.

The millimetre image of the Centaurus A nucleus by the Event Horizon Telescope reveals a highly collimated, asymmetrically edge-brightened jet. The source’s event horizon shadow should be visible at terahertz frequencies, consistent with the universal scale invariance of black holes.

Namba et al develop a new pipeline called MuSTA to enable the efficient assembly of transcriptome from long-read sequencing data of breast cancer samples. This method enables the authors to discover subtype-specific isoforms, find that fusion transcript structures depend on their genomic context and identify a double-hop fusion that results in aberrant expression of an endogenous retroviral gene.

Satoshi Narumi, Tomonobu Hasegawa and colleagues describe a new adrenal hypoplasia syndrome termed MIRAGE that is caused by mutations in the endosome fusion facilitator SAMD9. They find that patients with these mutations have severe growth restriction phenotypes, and they observe adaptation by aneuploidy, where there is accompanying protective loss of mutation-carrying chromosome 7.

The signaling through α7 nicotinic acetylcholine receptor (α7nAChR) in mouse macrophages has been revealed to enhance macrophage-macrophage interactions in the spleen and has a protective effect on the kidneys.