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Jones, A.

Publications and source records attributed to Jones, A..

At least 37 records · Page 2Linked to original sources

Genomic prediction of disease resistance provides a path to marker assisted restoration in a wetland foundation tree species

Tree species worldwide are under threat from non-native pathogens that impact forests and the ecosystem services they provide. Myrtle rust, caused by Austropuccinia psidii, is one example, first detected in Australia in 2010. This fungal pathogen infects immature tissue from a wide range of Myrtaceae hosts, including the wetland foundation species Melaleuca quinquenervia. Durable restoration action for this species would preferentially incorporate disease resistant individuals. Our aim for this study was to provide a molecular assay to identify and select resistant individuals and seed lots for restoration. We conducted artificial inoculation of a panel of seedlings and measured their immune responses to myrtle rust. We then performed whole genome sequencing (3.2M common SNPs) and conducted a Genome Wide Association Study (N = 492), which revealed clusters of significantly associated SNPs in three chromosomal regions, including clusters of putative R genes. Associated SNPs were filtered to a panel of 1,049 for a highly accurate genomic prediction model (R = 0.83). This provides a relatively inexpensive approach to identifying resistant individuals or seed lots for restoration and a template for managing myrtle rust impacts while maintaining population genetic diversity.

plant biology↗

Cell Cycle Arrest of a "Zippering" Epithelial Cell Cluster Shapes the Face and is Disrupted in Craniofacial Disorders

Facial features identify individuals, but the mechanisms shaping the human face remain elusive. Orofacial clefting (OFC), the most common craniofacial abnormality, results from failed fusion of the facial prominences that is in part caused by persistence of the cephalic epithelium. Here we uncover the identity, behaviors, and molecular blueprints of a novel craniofacial epithelial population, the Zippering Lambda (ZL), which mediates prominence fusion and is characterized by cell cycle arrest in mouse and human embryos. Remarkably, cell cycle is unleashed in the ZL of Pbx1/2 and p63 mutant mice with OFC. Intersection of ZL-enriched genes with human OFC whole-genome sequencing datasets identifies ZFHX3 variants in affected individuals and cephalic epithelial Zfhx3 deletion causes murine OFC. ZFHX3 and PBX1 genetically interact and synergistically regulate cell cycle inhibitor genes within a complex in embryonic faces. Collectively, we deconstruct new mechanisms that pattern the face, connecting cell cycle arrest to developmental tissue fusion.

developmental biology↗

Pharmacological inhibition of all known major inward cationic currents does not block the induction of spreading depolarizations

Spreading depolarization (SD) is a wave of profound cellular depolarization that propagates across central nervous system tissue and causes a near-complete collapse of ionic gradients. Implicated in neuropathologies including seizures, migraine with aura, traumatic brain injury, and stroke, SD is experimentally induced in animals by electrical stimulation, mechanical injury, hypoxia, elevated extracellular potassium, and various other techniques. Despite extensive research, the mechanisms underlying SD initiation remain unclear. Prior research in rodents found that simultaneously blocking sodium, calcium, and glutamatergic (AMPA and NMDA) channels prevents SD induction whereas inhibiting any two of these three currents is insufficient. This suggests that SD induction could be a product of overstimulation of any single known inward cationic current. However, some researchers propose that SD induction occurs via an unknown "SD channel." To further explore the role of known inward cationic currents in SD induction, we applied high potassium to two biological models, namely zebrafish and mice. First, we developed a novel ex vivo zebrafish model to assess SD induction in the optic tectum. Using KCl microinjection and DC local field potential recordings, we found that inhibition of sodium, calcium, and glutamatergic channels significantly decreased SD amplitude but never blocked SD induction in the zebrafish optic tectum. Similar pharmacological experiments in hippocampal mouse slices (CA1 subregion) also confirmed that SDs persist despite the same pharmacological cocktail. These findings suggest that additional mechanisms beyond sodium, calcium, and glutamatergic signaling contribute to SD induction, supporting the hypothesis that a currently unknown channel is critical in SD physiology.

neuroscience↗

Charting the single cell transcriptional landscape governing visual imprinting.

Memory-related transcriptional events in brain remain poorly understood. Visual imprinting is a form of learning in which young animals develop preferences through early exposure to specific stimuli. In chicks, visual imprinting memory is stored in the intermediate medial mesopallium (IMM) of the forebrain. To investigate learning-associated molecular changes, we performed single-nucleus RNA sequencing of the left IMM in strongly imprinted chicks and untrained controls. This analysis generated the first classification of cells composing the IMM, identifying as a result over 30 cell clusters with distinct transcriptional differences putatively linked to memory formation, nearly half of them in long non-coding RNAs (lncRNAs). Follow-up analysis on selected genes, confirmed that the gene expression levels of two lncRNAs and protein levels of FOXP2, RORA (transcription factors), LUC7L (splicing factor), and ROBO1 (axon guidance molecule) correlate with memory strength, reflecting either innate learning potential or imprinting experience. Additionally, among the confirmed lncRNAs, the brain- and avian-specific lncRNA ENSGALG00010007489 is enriched in the nuclei of specific glutamatergic clusters and its association with imprinting was further confirmed through quantitative multi-probe in situ hybridization. These findings offer the first single-cell resolution map of transcriptional changes underlying memory formation in the avian brain.

neuroscience↗

Host adaptation and genome evolution of the broad host range fungal rust pathogen, Austropuccinia psidii

Rust diseases on plants are caused by fungi in the order Pucciniales. Typically, rust fungi have narrow host specificity however the pandemic biotype of Austropuccinia psidii has an unusually broad host range causing disease on over 480 myrtaceous species globally. We assembled and analysed a fully phased chromosome-level genome for the pandemic A. psidii and addressed key outstanding questions of its infection biology. Our research revealed a conserved rust fungal karyotype of 18 haploid chromosomes, in line with fungi for distantly related cereal rusts. We observed chromosomal re-assortment between the two nuclei, with one nucleus carrying 19 and the other 17 chromosomes. The synteny of universal single-copy orthologs is mostly maintained with the distantly related rust fungus Puccinia graminis f. sp. tritici. In contrast, nucleotide composition and methylation profiles of A. psidii are distinct compared to rust fungi with smaller genome sizes that have not undergone massive transposable element expansions. Our analysis of mating type loci supports a tetrapolar mating system for A. psidii with a novel finding of expanded numbers of pheromone peptide precursors. We show that infection dynamics of A. psidii are consistent on four different susceptible host species separated by 65 mya of evolution and that transcriptional regulation during infection reveals two distinct waves of gene expression in early and late infection, including allele-specific expression of candidate effectors. Together, these findings enhance the understanding of the genome biology and pathology of A. psidii, while also providing a valuable resource for future research on this serious rust pathogen.

microbiology↗

Prenatal alcohol exposure promotes nerve injury-induced pathological pain following morphine treatment via NLRP3-mediated peripheral and central proinflammatory immune actions.

Adverse in-utero conditions may exert a lifelong impact on neuroimmune function. Our prior work showed that prenatal alcohol exposure (PAE) increases pathological pain sensitivity (allodynia) following peripheral sciatic nerve injury. While the immune mechanism(s) of PAE-induced immune dysfunction are poorly understood, prior studies implicated the involvement of Toll-like receptor 4 (TLR4) and the nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasomes. Interestingly, emerging data suggest a surprising overlap of spinal glial proinflammatory activation via the TLR4-NLRP3-interleukin (IL)-1{beta} axis due to opioid treatment in nerve-injured non-PAE rodents. Considering this preclinical evidence, we explored whether PAE poses a risk factor in creating proinflammatory immune bias consequent to opioid (morphine) exposure. We hypothesized that under nerve injury conditions, PAE may interact with morphine, promoting peripheral and CNS proinflammatory factors in a NLRP3-dependent manner. Using a minor nerve injury model in adult mice, we demonstrate that PAE prolongs the chronicity of ongoing allodynia in both sexes, with a more pronounced effect observed in male mice. Our study shows that PAE amplifies proinflammatory responses at the injury site and the spinal cord, driving morphine-prolonged allodynia through NLRP3 inflammasome activation. Furthermore, high mobility group box 1 (HMGB1), a well-established pain-promoting TLR4 agonist, is elevated in allodynic PAE mice. NLRP3 inhibitor, MCC950, effectively reverses morphine-induced allodynia and reduces Caspase-1 activity, IL-1{beta}, and related proinflammatory factors. Although few sex-specific effects were observed, our data convincingly support that PAE and morphine interactions ultimately converge on NLRP3-driven mechanisms in both sexes. Together, this study suggests that PAE modulates later-life neuroimmune function and provides critical insights into immune regulators underlying PAE-induced biological vulnerability to pathological pain processing and adverse effects of opioids.

neuroscience↗

Study buddy learning is associated with academic success in undergraduate science courses

This study reports on the outcomes of a formal peer-learning program for undergraduate science students. We implemented a cohort-based study buddy program in which high-scoring students (mentors) and lower-scoring peers (proteges) were invited to form study groups based on their first assessment scores in a given course. We then compared the performance of participants versus non-participants on subsequent assessments, while examining separately the effects for mentors and proteges. Results showed similar participation benefits for students in both mentor and protege roles. These findings emphasize the value of reducing barriers to collaborative learning in higher education and highlight the study buddy program as a cost-effective and scalable approach to enhance students educational experiences.

scientific communication and education↗

Elucidating tissue and sub-cellular specificity of the entire SUMO network reveals how stress responses are fine-tuned in a eukaryote

SUMOylation is essential in plant and animal cells, but it remains unknown how SUMO components act in concert to modify specific targets in response to environmental stresses. In this study we characterise every SUMO component in the Arabidopsis root to create the first complete SUMO Cell Atlas in eukaryotes. This unique resource reveals wide spatial variation, where SUMO proteins and proteases have sub-functionalized in both their expression and subcellular localisation. During stress SUMO conjugation is mainly driven by tissue specific regulation of the SUMO E2 ligase. Stress-specific modulation of the SUMO pathway reveals unique combinations of Proteases being targeted for regulation in distinct root tissues by salt, osmotic and biotic signals. Our SUMO Cell Atlas resources reveal how this PTM influences cellular and tissue scale adaptations during root development and stress responses. We provide the first comprehensive study elucidating how multiple stress inputs can regulate an entire PTM system.

plant biology↗

Vascular Biomechanics and Brain Biochemistry in Aged and Alzheimer's Disease Mouse Models

Age-related vascular changes accompany or precede the development of Alzheimers disease (AD) pathology. The comorbidity of AD and arterial stiffening may suggest that vascular changes have a pathogenic role. Carotid artery mechanics and hemodynamics have been associated with age-related cognitive decline. However, the impact of hemodynamics and vascular mechanics on regional vulnerability within the brain have not been thoroughly explored. Despite the venous systems role in transport, the impact of age-related alterations of the brain venous circulation on cognitive impairment is much less understood compared to the arterial system. By studying vascular mechanics and the resulting spatially-resolved brain lipids in young and aged AD mice, we can determine the relationship between vascular stiffening and brain function. Young and aged female 3xTg mice and age-matched controls were imaged using a combination of ultrasound and mass spectrometry. Wall shear stress varied across age and AD (p<0.05). The circumferential cyclic strain values for the carotid arteries and the WSS values for the jugular veins between groups were measured but were not statistically significant. Both mean velocity and pulsatility index (PI) varied across age and AD (p<0.05). Liquid chromatography mass spectrometry (LC-MS) of brain tissue identified several lipids and metabolites with statistically significant quantities (p<0.05). The fold change was computed for young AD vs. young control, aged AD vs. aged control, aged control vs. young control, and aged AD vs. young AD. The abundance of several lipid headgroups changed significantly with respect to age and AD. Phosphatidylcholines (PC), phosphatidylethanolamines (PE), cardiolipins (CL), phosphatidylserines (PS), and lysophosphatidylcholines (LPC) have been shown to decrease with AD in previous studies. However, we observed a statistically significant increase in PC, PE, CL, PS, and LPC in the aged 3xTG mouse model compared to aged controls. Hexosylceramides (HexCer), ceramides (CER) and sphingomyelin (SM), classes of sphingolipids; lysophosphatidylethanolamine (LPE), a class of phospholipids; and onogalactosyl diglycerides (MGDG), a class of glycerolipids, have been shown to increase with AD in previous studies which aligns with the statistically significant increase of LPC, HexCer, CER, SM, LPE, and MDG observed in the aged 3xTg group compared to controls in this work. Combining both ultrasound imaging and mass spectrometry, we were able determine significant differences in the vascular biomechanics and brain biochemistry seen with aging and AD.

neuroscience↗

Stathmin 1 regulates mitophagy and cellular function in hematopoietic stem cells

Stathmin 1 is a cytoplasmic phosphoprotein that regulates microtubule dynamics via promotion of microtubule catastrophe and sequestration of free tubulin heterodimers. Stathmin 1 is highly expressed in hematopoietic stem cells (HSCs), and overexpressed in leukemic cells, however its role in HSCs is not known. Herein, we found that loss of Stathmin 1 is associated with altered microtubule architecture in HSCs, and markedly impaired HSC function. Transcriptomic studies suggested alterations in oxidative phosphorylation in Stmn1-/- HSCs, and further mechanistic studies revealed defective mitochondrial structure and function in the absence of Stathmin 1 with increased ROS production. Microtubules associate with mitochondria and lysosomes to facilitate autophagosome formation and mitophagy, and indeed we found that this critical mitochondrial quality control process is impaired in Stathmin 1-deficient HSCs. Finally, stimulation of autophagy improved the colony forming ability of Stmn1-/- hematopoietic stem and progenitor cells. Together, our data identify Stathmin 1 as a novel regulator of mitophagy and mitochondrial health in HSCs. Key PointsO_LIThe microtubule regulating protein Stathmin 1 is highly expressed in HSPCs and promotes normal microtubule architecture. C_LIO_LILoss of Stathmin 1 in HSPCs leads to impaired autophagy with abnormal mitochondrial morphology, decreased respiratory capacity, and impaired cellular function. C_LI

cell biology↗

Epigenomic insights into extreme longevity in the world's oldest terrestrial animal, Jonathan

Giant tortoises exhibit exceptional longevity, often exceeding the human lifespan. To understand the genomic and epigenomic basis of their longevity, awe analyzed the DNA sequence and methylome of Jonathan, an Aldabra giant tortoise (Aldabrachelys gigantea), estimated to be 192 years old. Relative to other giant tortoises (Aldabrachelys gigantea and Chelonoidis abingdonii), we found Jonathan has gene variants in pathways associated with aging, including DNA repair and telomere regulation. Consistent with his advanced age, Jonathan has significant age-related changes in DNA methylation and methylation entropy, compared with a 5-year-old Aldabra individual. Notably, we found that low entropy regions in Jonathans methylome were enriched for genes involved in the electron transport chain. This suggests that high-fidelity transcription of these genes may be crucial for extreme longevity. With this data, we propose a model for aging, that links efficient mitochondrial energy production with nuclear maintenance of low methylation entropy.

genomics↗

DNA origami directed integration of colloidal nanophotonic materials with silicon photonics

Incorporation of colloidal quantum emitters into silicon-based photonic devices would enable major advances in quantum optics. However, deterministic placement of individual sub-10 nm colloidal particles onto micron-sized photonic structures with nanometer-scale precision remains an outstanding challenge. Here, we introduce Cavity-Shape Modulated Origami Placement (CSMOP) that leverages the structural programmability of DNA origami to precisely deposit colloidal nanomaterials within lithographically-defined resist cavities. CSMOP enables clean and accurate patterning of origami templates onto photonic chips with high yields. Soft-silicification-passivation stabilizes deposited origamis, while preserving their binding sites to attach and align colloidal quantum rods (QRs) to control their nanoscale positions and emission polarization. We demonstrate QR integration with photonic device structures including waveguides, micro-ring resonators, and bullseye photonic cavities. CSMOP therefore offers a general platform for the integration of colloidal quantum materials into photonic circuits, with broad potential to empower quantum science and technology.

bioengineering↗

Androgen stimulation rapidly reorganizes temporal 3D genome and epigenome states to trigger AR-mediated transcription in prostate cancer.

Androgen receptor (AR)-mediated transcription drives prostate cancer progression and remains a critical therapeutic target. AR activation by androgens triggers nuclear translocation, DNA binding at AR regulatory elements (AREs) and transcription initiation. This process involves co-factors such as FOXA1, epigenetic modifications, and 3D chromatin interactions. However, the temporal coordination of these events during AR-mediated transcription remains poorly understood. Using a time-course androgen stimulation model in prostate cancer cells, we integrated temporal multi-omics data within the MOFA+ framework to dissect AR-mediated transcriptional dynamics. Our analysis revealed that rapid AR binding at gene promoters is crucial for initiating nascent transcription of AR target genes. We identified H3K27 acetylation at flanking AREs, pre-marked by constitutive FOXA1 binding, occurs prior to AR recruitment. Additionally, androgen stimulation induced a temporal early shift in nascent transcription from MYC to AR target genes, associated with transient disruption of 3D chromatin interactions. Finally, we showed that CRISPR-mediated inhibition of AR-associated chromatin contacts suppresses distal linked target genes, demonstrating that dynamic genome architecture is functionally required for AR-driven transcription. Together these findings uncover the dynamic reorganization of 3D chromatin structure and transcription factor binding post-androgen stimulation, resulting in distinct temporal epigenomic states. This work provides new insights into the mechanisms governing AR-mediated transcriptional activation in prostate cancer and highlights the interplay between MYC and AR in regulating transcription in hormone-driven cancers.

genomics↗

Long-read genomics reveal extensive nuclear-specific evolution and allele-specific expression in a dikaryotic fungus

Phased telomere to telomere (T2T) genome assemblies are revolutionising our understanding of long hidden genome biology "dark matter" such as centromeres, rDNA repeats, inter-haplotype variation, and allele specific expression (ASE). Yet insights into dikaryotic fungi that separate their haploid genomes into distinct nuclei is limited. Here we explore the impact of dikaryotism on the genome biology of a long-term asexual clone of the wheat pathogenic fungus Puccinia striiformis f. sp. tritici. We use Oxford Nanopore (ONT) duplex sequencing combined with Hi-C to generate a T2T nuclear-phased assembly with >99.999% consensus accuracy. We show that this fungus has large regional centromeres enriched in LTR retrotransposons, with a single centromeric dip in methylation that suggests one kinetochore attachment site per chromosomes. The centromeres of chromosomes pairs are most often highly diverse in sequence and kinetochore attachment sites are not always positionally conserved. Each nucleus carries a unique array of rDNAs with >200 copies that harbour nucleus-specific sequence variations. The inter-haplotype diversity between the two nuclear genomes is caused by large-scale structural variations linked to transposable elements. Nanopore long-read cDNA analysis across distinct infection conditions revealed pervasive allele specific expression for nearly 20% of all heterozygous gene pairs. Genes involved in plant infection were significantly enriched in ASE genes which appears to be mediated by elevated CpG gene body methylation of the lower expressed pair. This suggests that epigenetically regulated ASE is likely a previously overlooked mechanism facilitating plant infection. Overall, our study reveals how dikaryotism uniquely shapes key eukaryotic genome features.

genomics↗

Identification of potent HSV antivirals using 3D bioprinted human skin equivalents

Herpes simplex virus (HSV) infection has worldwide public health concerns and lifelong medical impacts. The standard therapy, acyclovir, has limited efficacy in preventing HSV subclinical virus shedding, and drug resistance occurs in immunocompromised patients, highlighting the need for novel therapeutics. HSV manifests in the skin and mucosal epithelium. Here, we found acyclovir significantly less effective in skin-derived keratinocytes than donor-matched fibroblasts. To recapitulate in vivo tissue architecture, we 3D bioprinted human skin equivalents (HSE) in a 96-well plate format amenable for antiviral screening and preclinical testing. We screened a library of 738 compounds with broad targets and mechanisms of action and identified potent antivirals, including 23 known or experimental HSV treatments, validating the translational relevance of our assay. Unlike acyclovir, antivirals against HSV helicase/primase or host replication pathways displayed similar potency across cell types and donor sources in 2D and 3D models. Our 3D bioprinted platform allowed for integrating patient-derived cells and incorporating genetic variability early in drug development. The reduced potency in keratinocytes helps explain the limited benefit acyclovir and its congeners play in reducing sexual transmission. These data indicate that the 3D bioprinted HSE assay platform provides a more physiologically relevant approach to identifying potential antivirals for HSV. One Sentence SummaryHigh-throughput screen using 3D bioprinted human skin equivalents to identify antivirals against HSV and evaluate cell-type specific effects.

bioengineering↗

Reduced regulatory complexity associated with the evolutionary transition to sociality from cockroaches to termites despite evolutionary parallels with Hymenoptera

The degree of phenotypic diversity within social species has previously been associated with more complex genetic regulation both in cis and trans contexts. Transcription factors (TFs) being key to genetic regulation, have been studied in the origins of eusociality in Hymenoptera (bees, ants and wasps) but less so in Blattodea (cockroaches and termites). Here we show that the social transition in Blattodea, from cockroaches to termites, displays similar patterns of regulatory change to those found in Hymenoptera. Specifically, by analysing 3 cockroach and 5 termite genomes, we find more TF families with relaxed selection compared to intensified selection and lineage-specific gene family expansions in termites, which has also been reported in Hymenoptera. We also find that genes under selection support neotenic caste determination. We find there are key differences in Blattodea TF regulation in comparison with Hymenoptera with contractions in TF gene families and no compensatory change in TF DNA binding motifs either in frequency or diversity in TF promoter regions. Furthermore, we show that an increase in social complexity leads to greater diversity in TF activating domains, one of the evolutionary and structural building blocks of TFs, meanwhile, DNA-binding domains, undergo very little change. This study highlights similarities in social transitions between Hymenoptera and Blattodea, with evidence of large changes in transcriptional regulation followed by lineage specific adaptations. Our results indicate that the transcriptional diversity linked to social complexity is not attributable to transcription factors, but is instead likely driven by an alternative mechanism.. Significance statementIt has been widely reported that increased phenotypic complexity, particularly arising from social transitions, is often accompanied by increased regulatory complexity followed by lineage-specific adaptations. While extensively studied in Hymenoptera (bees, ants, and wasps), it has been less explored in Blattodea (cockroaches and termites). By examining the evolution of transcription factors across Blattodea, we investigated the regulatory changes associated with this social transition. Our study reveals that increased social complexity in Blattodea is accompanied by a reduction in regulatory complexity, including decreases in transcription factor numbers and no compensatory change in TF promoter binding site diversity or regulation. This study highlights that social transitions in Blattodea and Hymenoptera share a common pattern of large regulatory changes followed by lineage-specific adaptations.

evolutionary biology↗

Genomics and resistance assays inform the management of two tree species being devastated by the invasive myrtle rust pathogen

Myrtle rust is a plant disease caused by the invasive fungal pathogen Austropuccinia psidii (G. Winter) Beenken, which has a global host list of 480 species. It was detected in Australia in 2010 and has caused the rapid decline of native Myrtaceae species, including rainforest trees Rhodamnia rubescens (Benth.) Miq. (scrub turpentine) and Rhodomyrtus psidioides (G.Don) Benth. (native guava). Ex situ collections of these species have been established, with the goal of preserving remaining genetic variation. Analysis of reduced representation sequencing (DArTseq; n = 444 for R. rubescens and n = 301 for R. psidioides) showed genetic diversity is distributed along a latitudinal gradient across the range of each species. A panel of samples of each species (n = 27 for R. rubescens and n = 37 for R. psidioides) were resequenced at genome scale, revealing large historical e]ective population sizes, and little variation among individuals in inferred levels of deleterious load. In Rhodamnia rubescens, experimental assays (n = 297) identified individuals that are putatively resistant to myrtle rust. This highlights two important points: there are tangible pathways to recovery for species that are highly susceptible to rust via a genetically informed breeding program, and there is a critical need to act quickly before more standing diversity is lost.

genomics↗

Environmental cues influence timing and location ofconstruction activity in a beaver damming complex

Beavers are famous for building extensive damming complexes1, which can extend over kilometer-scale distances2 and persist for centuries3. Dams have major impacts on their surrounding environment, including effects on the hydrology, geomorphology, and ecosystems of the area4. Current understanding of how the environment in turn affects beavers building activity centers on the single auditory cue of running water, based primarily on captive studies14,15. Observational challenges have limited a more detailed picture of the full feedback loop between beavers and their environment. Here we describe the detailed progress of new construction by 20 beaver colonies in northwest Montana, through field studies using drones to obtain surveys with spatial and temporal resolution each three orders of magnitude finer than typically reported5-13. We show that both the timing and location of beaver construction activity are influenced by environmental factors. Initiation of trail clearing, a stage preceding dam building, was associated with a narrow range of stream flow rates. Beavers preferentially built in locations associated with preexisting canals. These results emphasize the importance of non-dam elements in the beavers construction and its coordination across the colony, and point to environmental feedback processes that may span across years and unrelated colonies.

animal behavior and cognition↗