The authors have retracted this article.After conducting replication experiments and reanalysing the original data, the authors discovered that the voltage imaging results, as presented in Figs.3a through 3f and Figs.4a andb, and discussed in the "Neurons gain cross-modal activation" section, are not reproducible.Additional voltage imaging work by the authors and their collaborators, for the conditions associated with Figs.3a through 3d, has not produced robust signals.Furthermore, errors in the pipeline originally used for data analysis could have led to the contamination of the F/F 0 data.A complete reanalysis by the authors of the voltage imaging data independently from the original pipeline did not replicate the original analysis.Although the authors have replicated the behavioural and connectomic data and consider that the general conclusions of the article are substantiated, the authors have no confidence in the voltage imaging data.

ABSTRACT This lecture speaks about remembrance, about how we remember and, mostly, about how we forget features of the slave trade – to our peril, and to that of the international community. Such forgetting or obliteration of the past denigrates our perceptions of the present. However, whatever is obliterated by memory never really disappears. It submerges, then resurfaces. It re-emerges with sturdy determination to carve and sculpt our current existence. Hence, this lecture is entitled ‘The Re-emergence of the (Internal) Slave Trade’. These remarks largely derive from the author’s persistent delving into international criminal law as a practitioner, a scholar and as an eternal student. They also emanate from her voice, as a descendant of enslaved ancestors.

MECOM encodes a developmental and haematopoietic transcription factor associated with a rare early-onset syndrome including bone marrow failure, skeletal and other congenital anomalies. Heterozygous de novo variants are the primary cause. We previously identified MECOM as a candidate gene for paediatric pulmonary arterial hypertension (PAH) using trio exome sequencing. To test the role of MECOM in paediatric PAH and further define the clinical phenotype of MECOM-associated syndrome, we queried GeneMatcher and screened rare disease databases for individuals with predicted deleterious MECOM variants. We analysed the clinical spectrum of patients, performed protein modelling of genetic variants and assessed cardiopulmonary expression. We identified 15 individuals with MECOM variants, including 11 unrelated probands and 8 de novo variants. 11 individuals had severe or mild thrombocytopenia, 9 had skeletal issues, 8 had cardiac anomalies, 6 had PAH and 10 had additional conditions. Three were diagnosed in utero and died in the neonatal period. All missense variants map to the zinc finger 6 or zinc finger 8/9 region, a known hotspot for MECOM-associated syndrome. Protein modelling predicted that both regions are DNA-binding, and that the variants may interfere with binding to a VEGFR2/KDR enhancer. Data from LungMAP showed that MECOM is primarily expressed in pulmonary arterial endothelial cells. Rare MECOM variants are associated with early-onset syndromic PAH. PAH monitoring should be considered for all individuals with rare MECOM variants. We speculate that the pathogenetic mechanism for PAH and cardiac defects may be impaired VEGFR2/KDR signalling.

The use of monoclonal fragments antigen binding (Fabs) is a prevalent methodology facilitating protein structure determination via both crystallography and cryo-EM. The development of a synthetic Fab against the BRIL domain improved the accessibility of this approach, providing a general fiducial applicable to any protein of interest via the simple curation of a BRIL fusion protein. Here, we document the generation of a T7 Express ΔcybC strain allowing contaminant-free bacterial expression of the synthetic anti-BRIL Fab BAG2. We also report the crystal structure of BAG2 in complex with native cytochrome b562, a complex arising from expression in canonical Escherichia coli strains.

TRIM21 is a multifunctional E3 ubiquitin ligase and intracellular antibody receptor, yet its role during viral infection remains unclear, with reports describing both antiviral and proviral activities. Here, we show that TRIM21 regulates influenza infection in an expression-dependent manner by functioning as a molecular rheostat rather than a binary restriction factor. This graded activity of TRIM21, which leads to both suppression and promotion of influenza replication, couples linkage-specific ubiquitination of viral nucleoprotein with modulation of innate immune signaling. Additionally, loss of TRIM21 unmasks a compensatory antiviral program centered on PRKDC, which is a ubiquitination target of TRIM21. This positions PRKDC as a latent restriction factor selectively engaged when primary TRIM21 control is lost. Together, these findings reveal a hierarchical and plastic antiviral network in which TRIM21 sets an adjustable threshold for host defense while restraining secondary restriction pathways. This framework highlights the sophisticated layers of regulation of the host ubiquitin-mediated antiviral immunity.

Mitotic fidelity requires proper chromosome alignment at the spindle equator, a process known as chromosome congression, mediated by well-established protein networks. Although RNA-binding proteins (RBPs) and non-coding RNAs (ncRNAs) have been implicated in cell division, their functional interplay remains unclear. Here, we show that RSRC2, a poorly characterized RBP, is essential for proper cell division through its interaction with the long ncRNA C1QTNF1–AS1. Loss of either RSRC2 or C1QTNF1–AS1 causes mitotic defects. RSRC2 associates with distinct protein sets involved in splicing and centrosome biogenesis, regulating mitotic gene splicing and maintaining centriole integrity. RSRC2 depletion impairs recruitment of the centrosomal scaffold proteins PCNT and CDK5RAP2, which are essential for organizing microtubules to form the mitotic spindle. While C1QTNF1–AS1 loss does not alter RSRC2 expression or its global interactome, it reduces RSRC2 localization at the centrosome. We also find that C1QTNF1–AS1 directs RSRC2 to the centrosome, where RSRC2, in turn, promotes the recruitment of PCNT mRNA to the centrosome. Our study highlights the critical role of RNA–protein complexes in ensuring error-free mitosis and identifies RSRC2 as a multifunctional protein with dual roles in splicing and centrosome-associated RNA localization.

Splenic rupture is a recognized complication of acute Plasmodium falciparum and Plasmodium vivax malaria, but the risk of splenic rupture in chronic asymptomatic infections is unknown. In Timika, Papua, Indonesia, we determined the proportion of PCR-detectable asymptomatic peripheral parasitemia in patients undergoing trauma-related splenectomy (2015-21) and found it was more than twice the proportion compared to a 2013 household survey of the general population (87.9% [29/33] vs 38.6% [697/1807]; P < .0001). Our findings suggest asymptomatic parasitemia with either P. falciparum or P. vivax is associated with splenic rupture following trauma, pointing toward an additional consequence of chronic infection in malaria-endemic areas.

Abstract Supermassive black hole (SMBH) growth plausibly occurs via runaway astrophysical black hole mergers in nuclear star clusters that form intermediate mass black hole seeds at high redshifts. Such a model yields an order-of-magnitude higher rate of tidal disruption events than that of compact-object captures. Our prediction, normalized to our proposed resolution of SMBH seeding, yields detectable tidal disruption event rates at high redshift. The resulting dense gas cocoons generate compact galactic nuclei, each incorporating a central, massive, black hole star, with comparable masses in gas, stars, and massive black holes within a scale of around a parsec as inferred from the various Little Red Dot spectral signatures.