Unexpected Complexity Research Articles

Impact of COVID-19 on women leadership in Saudi higher education institutions

The COVID-19 epidemic caused unexpected complications, complexities and challenges in higher educational institutions (HEIs). In order to promote and strengthen the role of women leadership, this study aimed to clarify the unique challenges faced by female leaders at Saudi HEIs during the epidemic, find possible solutions to these challenges, and provide policy as well as management implications. A systematic literature review (SLR) was conducted, examining 27 records (i.e., research papers, articles and conference studies). The data were qualitatively analysed and categorized based on themes like challenges faced, opportunities recognized, and solutions proposed. Findings highlighted women leaders in Saudi HEIs grappled with multiple challenges, including technological barriers, cultural constraints, and increased workloads. Merging challenges with solvable strategies offers a forward-looking perspective, advocating for systemic changes that can shape a resilient and inclusive future for HEIs in Saudi Arabia.

Unexpected complexity of the Embioptera (Insecta) fauna of the Tuscan Archipelago (Italy), with the disambiguation of two species of Haploembia Verhoeff, 1904 and description of a new species of Embia Latreille, 1825

Very little is known about the Embioptera of the Tuscan Archipelago, and no specific study has been published from there on this insect order. The study of literature and new material has allowed us to identify the presence of four species of Embioptera in the Tuscan Archipelago: Haploembia solieri (Rambur, 1842), Haploembia tarsalis Ross, 1940 (which was reported for the first time in Italy), Embia ramburi Rimsky-Korsakov, 1905 and E. ilvana n. sp., which is described here. As regards the species of the genus Haploembia Verhoeff, 1904, some bio-ethological aspects and the global distribution of the two species present in the archipelago are discussed.

Revealing unexpected complex encoding but simple decoding mechanisms in motor cortex via separating behaviorally relevant neural signals.

In motor cortex, behaviorally relevant neural responses are entangled with irrelevant signals, which complicates the study of encoding and decoding mechanisms. It remains unclear whether behaviorally irrelevant signals could conceal some critical truth. One solution is to accurately separate behaviorally relevant and irrelevant signals at both single-neuron and single-trial levels, but this approach remains elusive due to the unknown ground truth of behaviorally relevant signals. Therefore, we propose a framework to define, extract, and validate behaviorally relevant signals. Analyzing separated signals in three monkeys performing different reaching tasks, we found neural responses previously considered to contain little information actually encode rich behavioral information in complex nonlinear ways. These responses are critical for neuronal redundancy and reveal movement behaviors occupy a higher-dimensional neural space than previously expected. Surprisingly, when incorporating often-ignored neural dimensions, behaviorally relevant signals can be decoded linearly with comparable performance to nonlinear decoding, suggesting linear readout may be performed in motor cortex. Our findings prompt that separating behaviorally relevant signals may help uncover more hidden cortical mechanisms.

Signature of systemic rotation in 21 galactic globular clusters from APOGEE-2

Context. Traditionally, globular clusters (GCs) have been assumed to be quasi-relaxed non-rotating systems, characterized by spherical symmetry and orbital isotropy. However, in recent years, a growing set of observational evidence has been unveiling an unexpected dynamical complexity in Galactic GCs. Indeed, kinematic studies have demonstrated that a measurable amount of internal rotation is present in many present-day GCs. Aims. The objective of this work is to analyse the APOGEE-2 value-added catalog (VAC) DR17 data of a sample of 21 GCs to extend the sample exhibiting signatures of systemic rotation and better understand the kinematic properties of GCs overall. Also, we aim to identify the fastest rotating GC from the sample of objects with suitable measurements. Methods. From the sample of 23 GCs included in this work, the presence of systemic rotation was detected in 21 of the GCs, using three different methods. All these methods use the radial velocity referred to the cluster systemic velocity (Ṽr). Using the first method, it was possible to visually verify the clear-cut signature of systemic rotation; whereas using the second and third methods, it was possible to determine the amplitude of the rotation curve (Arot) and the position angle (PA) of the rotation axis. Results. This study shows that 21 GCs have a signature of systemic rotation. For these clusters, the rotation amplitude and the position angle of the rotation axis (PA0) have been calculated. The clusters cover a remarkable range of rotational amplitudes, from 0.77 km s−1 to 13.85 km s−1.

Schizophrenia genomics: genetic complexity and functional insights.

Determining the causes of schizophrenia has been a notoriously intractable problem, resistant to a multitude of investigative approaches over centuries. In recent decades, genomic studies have delivered hundreds of robust findings that implicate nearly 300 common genetic variants (via genome-wide association studies) and more than 20 rare variants (via whole-exome sequencing and copy number variant studies) as risk factors for schizophrenia. In parallel, functional genomic and neurobiological studies have provided exceptionally detailed information about the cellular composition of the brain and its interconnections in neurotypical individuals and, increasingly, in those with schizophrenia. Taken together, these results suggest unexpected complexity in the mechanisms that drive schizophrenia, pointing to the involvement of ensembles of genes (polygenicity) rather than single-gene causation. In this Review, we describe what we now know about the genetics of schizophrenia and consider the neurobiological implications of this information.

Designing Plastrons for Underwater Bubble Capture: From Model Microstructures to Stochastic Nanostructures.

Bubbles and foams are often removed via chemical defoamers and/or mechanical agitation. Designing surfaces that promote chemical-free and energy-passive bubble capture is desirable for numerous industrial processes, including mineral flotation, wastewater treatment, and electrolysis. When immersed, super-liquid-repellent surfaces form plastrons, which are textured solid topographies with interconnected gas domains. Plastrons exhibit the remarkable ability of capturing bubbles through coalescence. However, the two-step mechanics of plastron-induced bubble coalescence, namely, rupture (initiation and location) and subsequent absorption (propagation and drainage) are not well understood. Here, the influence of 1) topographical feature size and 2) gas fraction on bubble capture dynamics is investigated. Smaller feature sizes accelerate rupture while larger gas fractions markedly improve absorption. Rupture is initiated solely on solid domains and is more probable near the edges of solid features. Yet, rupture time becomes longer as solid fraction increases. This counterintuitive behavior represents unexpected complexities. Upon rupture, the bubble's moving liquid-solid contact line influences its absorption rate and equilibrium state. These findings show the importance of rationally minimizing surface feature sizes and contact line interactions for rapid bubble rupture and absorption. This work provides key design principles for plastron-induced bubble coalescence, inspiring future development of industrially-relevant surfaces for underwater bubble capture.

Unexpected complexity in the molecular diagnosis of spastic paraplegia 11.

Spastic paraplegia 11 (SPG11) is the most prevalent form of autosomal recessive hereditary spastic paraplegia, resulting from biallelic pathogenic variants in the SPG11 gene (MIM *610844). The proband is a 36-year-old female referred for genetic evaluation due to cognitive dysfunction, gait impairment, and corpus callosum atrophy (brain MRI was normal at 25-years-old). Diagnostic approaches included CGH array, next-generation sequencing, and whole transcriptome sequencing. CGH array revealed a 180 kb deletion located upstream of SPG11. Sequencing of SPG11 uncovered two rare single nucleotide variants: the novel variant c.3143C>T in exon 17 (in cis with the deletion), and the previously reported pathogenic variant c.6409C>T in exon 34 (in trans). Whole transcriptome sequencing revealed that the variant c.3143C>T caused exon 17 skipping. We report a novel sequence variant in the SPG11 gene resulting in exon 17 skipping, which, along with a nonsense variant, causes Spastic Paraplegia 11 in our proband. In addition, a deletion upstream of SPG11 was identified in the patient, whose implication in the phenotype remains uncertain. Nonetheless, the deletion apparently affects cis-regulatory elements of the gene, suggesting a potential new pathogenic mechanism underlying the disease in a subset of undiagnosed patients. Our findings further support the hypothesis that the origin of thin corpus callosum in patients with SPG11 is of progressive nature.

Student and educator experiences of a student-led clinic in general practice.

Giving students more responsibility for real patients during medical school may help prepare them for their transition to clinical practice. Student-led clinics (SLCs) may facilitate this. Within SLCs, students take the lead role in delivering patient care while being supported and supervised by qualified clinicians. A general practice SLC was established in Dundee, with four final-year medical students and one GP involved in each clinic. This study aimed to explore students' and educators' experiences and perceptions of this SLC. This was an exploratory case study. Semi-structured interviews were conducted with 11 students and three educators, and 18 hours of observation were conducted over six clinics. Interview transcripts and fieldnotes were integrated and thematically analysed. Overall, students' and educators' experiences and perceptions were positive. Students thrived in their lead role in patient care, gaining a sense of empowerment and developing confidence in their abilities. Both students and educators felt comfortable with students having this level of responsibility due to the students' stage of training and the supervision provided by educators. Teaching within the SLC involved individual discussions and group debriefs. Students felt a sense of belonging as a result of their relationships with their peers and educators. Challenges arose when the clinic ran behind schedule due to unexpected complex patients or lengthy individual discussions. The findings suggest that giving students responsibility for real patients is beneficial and feasible when adequate support is provided, and that it is possible for one GP to supervise multiple students successfully.

A pseudoautosomal glycosylation disorder prompts the revision of dolichol biosynthesis

Dolichol is a lipid critical for N-glycosylation as a carrier for activated sugars and nascent oligosaccharides. It is commonly thought to be directly produced from polyprenol by the enzyme SRD5A3. Instead, we found that dolichol synthesis requires a three-step detour involving additional metabolites, where SRD5A3 catalyzes only the second reaction. The first and third steps are performed by DHRSX, whose gene resides on the pseudoautosomal regions of the X and Y chromosomes. Accordingly, we report a pseudoautosomal-recessive disease presenting as a congenital disorder of glycosylation in patients with missense variants in DHRSX (DHRSX-CDG). Of note, DHRSX has a unique dual substrate and cofactor specificity, allowing it to act as a NAD+-dependent dehydrogenase and as a NADPH-dependent reductase in two non-consecutive steps. Thus, our work reveals unexpected complexity in the terminal steps of dolichol biosynthesis. Furthermore, we provide insights into the mechanism by which dolichol metabolism defects contribute to disease.

Critical analysis of polycyclic tetramate macrolactam biosynthetic gene cluster phylogeny and functional diversity.

Polycyclic tetramate macrolactams (PTMs) are bioactive natural products commonly associated with certain actinobacterial and proteobacterial lineages. These molecules have been the subject of numerous structure-activity investigations since the 1970s. New members continue to be pursued in wild and engineered bacterial strains, and advances in PTM biosynthesis suggest their outwardly simplistic biosynthetic gene clusters (BGCs) belie unexpected product complexity. To address the origins of this complexity and understand its influence on PTM discovery, we engaged in a combination of bioinformatics to systematically classify PTM BGCs and PTM-targeted metabolomics to compare the products of select BGC types. By comparing groups of producers and BGC mutants, we exposed knowledge gaps that complicate bioinformatics-driven product predictions. In sum, we provide new insights into the evolution of PTM BGCs while systematically accounting for the PTMs discovered thus far. The combined computational and metabologenomic findings presented here should prove useful for guiding future discovery.IMPORTANCEPolycyclic tetramate macrolactam (PTM) pathways are frequently found within the genomes of biotechnologically important bacteria, including Streptomyces and Lysobacter spp. Their molecular products are typically bioactive, having substantial agricultural and therapeutic interest. Leveraging bacterial genomics for the discovery of new related molecules is thus desirable, but drawing accurate structural predictions from bioinformatics alone remains challenging. This difficulty stems from a combination of previously underappreciated biosynthetic complexity and remaining knowledge gaps, compounded by a stream of yet-uncharacterized PTM biosynthetic loci gleaned from recently sequenced bacterial genomes. We engaged in the following study to create a useful framework for cataloging historic PTM clusters, identifying new cluster variations, and tracing evolutionary paths for these molecules. Our data suggest new PTM chemistry remains discoverable in nature. However, our metabolomic and mutational analyses emphasize the practical limitations of genomics-based discovery by exposing hidden complexity.

Peculiarities of the chemical enrichment of metal-poor stars in the Milky Way Galaxy

The oldest stars in the Milky Way are metal-poor with Fe/H $<$ -- 1.0, displaying peculiar elemental abundances compared to solar values. The relative variations in the chemical compositions among stars is also increasing with decreasing stellar metallicity, allowing for the pure signature of unique nucleosynthesis processes to be revealed. The study of the $r$-process is, for instance, one of the main goals of stellar archaeology and metal-poor stars exhibit an unexpected complexity in the stellar production of the $r$-process elements in the early Galaxy. In this work, we report the atmospheric parameters, main dynamic properties, and the abundances of four metal-poor stars: HE 1523-–0901, HD 6268, HD 121135, and HD 195636 (--1.5 $>$ Fe/H The abundances were derived from spectra obtained with the HRS echelle spectrograph at the Southern African Large Telescope, using both local and non-local thermodynamic equilibrium (LTE and NLTE) approaches, with the average error between 0.10 and 0.20 dex. Based on their kinematical properties, we show that HE 1523--0901 and HD 195636 are halo stars with typical high velocities. In particular, HD 121135 displays a peculiar kinematical behaviour, making it unclear whether it is a halo or an accreted star. Furthermore, HD 6268 is possibly a rare prototype of very metal-poor thick disk stars. The abundances derived for our stars are compared with theoretical stellar models and with other stars with similar metallicity values from the literature. HD 121135 is Al-poor and Sc-poor, compared to stars observed in the same metallicity range (--1.62 $>$ Fe/H $>$--1.12). The most metal-poor stars in our sample, HE 1523 -- 0901, HD 6268, and HD 195636, exhibit anomalies that are better explained by supernova models from fast-rotating stellar progenitors for elements up to the Fe group. Compared to other stars in the same metallicity range, their common biggest anomaly is represented by the low Sc abundances. If we consider the elements beyond Zn, HE 1523--0901 can be classified as an r-II star, HD 6268 as an r-I candidate, and HD 195636 and HD 121135 exhibiting a borderline $r$-process enrichment between limited-r and r-I star. Significant relative differences are observed between the $r$-process signatures in these stars.

Institutional complexity and consumer wellbeing: Navigating the conflicting logics of religion, state, and market during the COVID-19 pandemic

Institutional complexity arises when multiple institutional logics prescribe divergent and incompatible behaviors. Studies show that exposure to contradictory prescriptions of multiple logics may trigger identity tensions, strategic challenges, and legitimacy problems. We add to this research stream by exploring the implications of the incompatibility between religion and other logics on consumer wellbeing. Extant research reports a generally positive effect of religion on wellbeing but limits the analytical attention to the individual effects of religiosity. Viewing religion as part of an inter-institutional system, we seek to understand why religion and other institutional logics might come into a conflictual relationship with each other and destabilize wellbeing. We find that critical events, such as the COVID-19 pandemic, change the relative centrality of logics and prompt individuals to engage in incompatible behaviors. We also discuss how consumers manage the sudden and unexpected institutional complexity they face and seek to restore their wellbeing.

Integrated analyses reveal unexpected complex inversion and recombination in RH genes

AbstractPhenotype D-- is associated with severe hemolytic transfusion reactions and hemolytic disease of the fetus and newborn. It is typically caused by defective RHCE genes. In this study, we identified a D-- phenotype proband and verified Rh phenotypes of other 6 family members. However, inconsistent results between the phenotypic analysis and Sanger sequencing revealed intact RHCE exons with no mutations in the D-- proband, but the protein was not expressed. Subsequent whole-genome sequencing by Oxford Nanopore Technologies of the proband revealed an inversion with ambiguous breakpoints in intron 2 and intron 7 and copy number variation loss in the RHCE gene region. Given that the RHCE gene is highly homologous to the RHD gene, we conducted a comprehensive analysis using Pacific Biosciences long-read target sequencing, Bionano optical genome mapping, and targeted next-generation sequencing. Our findings revealed that the proband had 2 novel recombinant RHCE haplotypes, RHCE∗Ce(1-2)-D(3-10) and RHCE∗Ce(1-2)-D(3-10)-Ce(10-8)-Ce(3-10), with clear-cut breakpoints identified. Furthermore, the RH haplotypes of the family members were identified and verified. In summary, we made, to our knowledge, a novel discovery of hereditary large inversion and recombination events occurring between the RHD and RHCE genes, leading to a lack of RhCE expression. This highlights the advantages of using integrated genetic analyses and also provides new insights into RH genotyping.

Identification of X chromatin is modulated by complementary pathways in Drosophila melanogaster.

Drosophila melanogaster males have one X chromosome while females have two. This creates an imbalance in X:A gene dosage between the sexes. This imbalance is corrected by increasing transcription from male X-linked genes approximately 2-fold. This process involves the Male-Specific Lethal (MSL) complex, which is recruited to Chromatin Entry Sites (CES) and transcribed X-linked genes, where it modifies chromatin to increase expression. Repetitive sequences strikingly enriched in X euchromatin, the 1.688X satellite repeats, also promote recruitment of the MSL complex to nearby genes. Unlike CES, the 1.688X repeats do not recruit the MSL complex directly. The genetic architecture of recruitment by these DNA elements remains speculative. To facilitate dissection of the mechanism of recruitment, we developed a luciferase reporter system for recruitment of compensation to an autosome. The system was validated by knock down of genes known to participate in compensation. Knock down of factors genetically linked to X recognition reveals that 1.688X repeats recruit through a different mechanism than the CES. Our findings suggest that 1.688X repeats play a larger role during embryogenesis, whereas the contribution of 1.688X repeats and CES is equivalent later in development. Our studies also reveal unexpected complexity and potential interdependence of recruiting elements.

Spatially organized cellular communities form the developing human heart

The heart, which is the first organ to develop, is highly dependent on its form to function1,2. However, how diverse cardiac cell types spatially coordinate to create the complex morphological structures that are crucial for heart function remains unclear. Here we integrated single-cell RNA-sequencing with high-resolution multiplexed error-robust fluorescence in situ hybridization to resolve the identity of the cardiac cell types that develop the human heart. This approach also provided a spatial mapping of individual cells that enables illumination of their organization into cellular communities that form distinct cardiac structures. We discovered that many of these cardiac cell types further specified into subpopulations exclusive to specific communities, which support their specialization according to the cellular ecosystem and anatomical region. In particular, ventricular cardiomyocyte subpopulations displayed an unexpected complex laminar organization across the ventricular wall and formed, with other cell subpopulations, several cellular communities. Interrogating cell–cell interactions within these communities using in vivo conditional genetic mouse models and in vitro human pluripotent stem cell systems revealed multicellular signalling pathways that orchestrate the spatial organization of cardiac cell subpopulations during ventricular wall morphogenesis. These detailed findings into the cellular social interactions and specialization of cardiac cell types constructing and remodelling the human heart offer new insights into structural heart diseases and the engineering of complex multicellular tissues for human heart repair.

Type I interferons, inflammation, and fatigue in a longitudinal RNA study of women with breast cancer

BackgroundFatigue is a common side effect of cancer and its treatment and is thought to be driven in part by activation of the proinflammatory cytokine network. However, the cellular and molecular underpinnings of cancer-related fatigue (CRF) have not been determined, nor have immune pathways beyond inflammation been carefully investigated. The goal of this study was to examine the association between CRF and activation of canonical proinflammatory gene regulation pathways and Type I interferon (IFN) signaling pathways in breast cancer patients during and after treatment. MethodsWomen diagnosed with early-stage breast cancer (n = 181) completed assessments before and after treatment with radiation and/or chemotherapy and at 6, 12, and 18-month post-treatment follow-ups. Assessments included self-reported fatigue (Multidimensional Fatigue Symptom Inventory – Short Form) and expression of pre-specified sets of Type I IFN and pro-inflammatory immune response genes determined from mRNA sequencing of PBMCs. Mixed effect linear models examined changes in fatigue and immune gene expression over time and tested the hypothesis that fatigue would be associated with increased expression of Type I IFN and inflammatory response genes. ResultsThere were significant changes in fatigue and immune gene expression across the assessment period; all measures increased from pre- to post-treatment but showed diverging patterns over the follow-up, with declines in fatigue and persistent elevations in Type I IFN and proinflammatory gene expression. In mixed effect linear models, expression of Type I IFN response genes was elevated in association with fatigue across the assessment period, from pre-treatment to 18-month follow-up. In contrast, pro-inflammatory gene expression was associated with fatigue only at 6, 12, and 18-month follow-ups. Analyses controlling for changes in leukocyte subsets continued to show a significant association between fatigue and Type I IFN gene expression but reduced the time-dependent association with pro-inflammatory gene expression to non-significant. ConclusionsResults revealed unexpected complexity in the immune underpinnings of CRF and identify a novel role for IFN signaling as a robust contributor to this symptom before, during, and after treatment. Pro-inflammatory gene expression emerged as a predictor of fatigue later in the cancer trajectory, and that effect was primarily accounted for by a concurrent increase in monocyte prevalence.

Surface effect on the phase separation in thin liquid crystal film as seen from a mean-field approach

The effect of the interplay between attractive nonlocal surface interactions and attractive pair long-range intermolecular couplings on molecular structures of liquid crystals confined in thin cells with flat solid surfaces has been studied. It has been shown, in the framework of the extended McMillan′s mean field theory, that in the confined LC system a complex orientational and translational ordering of molecules can be induced. Several scenarios of the formation of local smectic A, nematic, and isotropic phases have been shown to coexist in a certain temperature range. Due to the nonlocality of the surface interaction, an unexpected complexity of the spatial arrangement of these local phases along the direction of the normal to the surface may exhibit itself.

Neutrophils: from IBD to the gut microbiota.

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract that results from dysfunction in innate and/or adaptive immune responses. Impaired innate immunity, which leads to lack of control of an altered intestinal microbiota and to activation of the adaptive immune system, promotes a secondary inflammatory response that is responsible for tissue damage. Neutrophils are key players in innate immunity in IBD, but their roles have been neglected compared with those of other immune cells. The latest studies on neutrophils in IBD have revealed unexpected complexities, with heterogeneous populations and dual functions, both deleterious and protective, for the host. In parallel, interconnections between disease development, intestinal microbiota and neutrophils have been highlighted. Numerous IBD susceptibility genes (such as NOD2, NCF4, LRRK2, CARD9) are involved in neutrophil functions related to defence against microorganisms. Moreover, severe monogenic diseases involving dysfunctional neutrophils, including chronic granulomatous disease, are characterized by intestinal inflammation that mimics IBD and by alterations in the intestinal microbiota. This observation demonstrates the dialogue between neutrophils, gut inflammation and the microbiota. Neutrophils affect microbiota composition and function in several ways. In return, microbial factors, including metabolites, regulate neutrophil production and function directly and indirectly. It is crucial to further investigate the diverse roles played by neutrophils in host-microbiota interactions, both at steady state and in inflammatory conditions, to develop new IBD therapies. In this Review, we discuss the roles of neutrophils in IBD, in light of emerging evidence proving strong interconnections between neutrophils and the gut microbiota, especially in an inflammatory context.

Autonomous and non-cell autonomous role of cilia in structural birth defects in mice.

Ciliopathies are associated with wide spectrum of structural birth defects (SBDs), indicating important roles for cilia in development. Here, we provide novel insights into the temporospatial requirement for cilia in SBDs arising from deficiency in Ift140, an intraflagellar transport (IFT) protein regulating ciliogenesis. Ift140-deficient mice exhibit cilia defects accompanied by wide spectrum of SBDs including macrostomia (craniofacial defects), exencephaly, body wall defects, tracheoesophageal fistula (TEF), randomized heart looping, congenital heart defects (CHDs), lung hypoplasia, renal anomalies, and polydactyly. Tamoxifen inducible CAGGCre-ER deletion of a floxed Ift140 allele between E5.5 to 9.5 revealed early requirement for Ift140 in left-right heart looping regulation, mid to late requirement for cardiac outflow septation and alignment, and late requirement for craniofacial development and body wall closure. Surprisingly, CHD were not observed with 4 Cre drivers targeting different lineages essential for heart development, but craniofacial defects and omphalocele were observed with Wnt1-Cre targeting neural crest and Tbx18-Cre targeting epicardial lineage and rostral sclerotome through which trunk neural crest cells migrate. These findings revealed cell autonomous role of cilia in cranial/trunk neural crest-mediated craniofacial and body wall closure defects, while non-cell autonomous multi-lineage interactions underlie CHD pathogenesis, revealing unexpected developmental complexity for CHD associated with ciliopathies.

Deep ancestry of Bornean hunter-gatherers supports long-term local ancestry dynamics

Borneo was a crossroad of ancient dispersals, with some of the earliest Southeast Asian human remains and rock art. The island is home to traditionally hunter-gatherer Punan communities, whose origins, whether of subsistence reversion or long-term foraging, are unclear. The connection between its past and present-day agriculturalist inhabitants, who currently speak Austronesian languages and have composite and complex genetic ancestry, is equally opaque. Here, we analyze the genetic ancestry of the northeastern Bornean Punan Batu (who still practice some mobile hunting and gathering), Tubu, and Aput. We find deep ancestry connections, with a shared Asian signal outgrouping modern and ancient Austronesian-ancestry proxies, suggesting a time depth of more than 7,500 years. They also largely lack the mainland Southeast Asian signals of agricultural Borneans, who are themselves genetically heterogeneous. Our results support long-term inhabitation of Borneo by some Punan ancestors and reveal unexpected complexity in the origins and dispersal of Austronesian-expansion-related ancestry.