Biology subjects

Robertson, F.

Publications and source records attributed to Robertson, F..

9 recordsLinked to original sources

bioRxiv2026

Social behaviour is a key determinant of virome diversity in New Zealand passerines

Wild birds are important reservoirs of viral diversity and can play key roles in the emergence and dispersal of infectious diseases. Their ability to harbour multiple infections without overt disease, combined with their mobility and ecological interactions, creates opportunities for viruses to spread across species and geographic regions. Despite this, the factors shaping avian viromes remain poorly understood, particularly in Aotearoa New Zealand, where endemic and introduced bird species coexist within a relatively isolated ecosystem. This study used metatranscriptomic sequencing to characterise the viromes of 443 endemic and introduced passerines sampled over four years within a shared ecological setting. A total of 217 viruses, representing 69 viral species across 14 families, were identified, including 54 previously undescribed viruses. Many were closely related to viruses reported from birds in Asia, North America, Europe and Australia, suggesting historical or ongoing viral exchange through migration, co-divergence or cross-species transmission. Introduced passerines harboured greater viral diversity than endemic species, while social behaviour was a key predictor of virome composition with flocking species exhibiting higher viral richness and diversity than solitary or pair-living taxa. In contrast, non-viral microbial communities were primarily shaped by host species and diet, indicating that viral communities are influenced by ecological processes distinct from those associated with the non-viral microbiome. These findings provide new insight into the ecological and behavioural drivers of avian viral diversity.

microbiology↗

bioRxiv2026

Orphan GPR84 facilitates uropod de-adhesion to terminate leukocyte diapedesis during inflammation

Leukocyte migration through venular walls is an essential component of effective immunity. While the key molecular players driving the initial steps of this response are known, the terminating signals remain unclear. Here, we have identified a conserved role for GPR84 family GPCRs in successful completion of the final stages of leukocyte extravasation through acutely inflamed vessels. The integration of high resolution intravital imaging with cell-specific genetics revealed that genetic deficiency of GPR84 orthologues in mice and Drosophila, results in defective detachment of transmigrating immune cells from vessel walls. Mechanistically, transcriptomics revealed GPR84-deficient neutrophils exhibit defective actin cytoskeletal regulation and cellular adhesion/de-adhesion. Consistent with this, our fly-murine pipeline shows that GPR84 supports localized and dynamic Rho activation to enable detachment of the immune cell uropod from vessel exit sites. Moreover, pharmacological blockade of GPR84 signaling dampened immune cell migration in multiple murine acute inflammatory settings. Collectively, our findings present GPR84 as a novel physiological regulator of immune cell extravasation that is amenable to therapeutic targeting for modulating leukocyte infiltration into inflamed tissues. SummaryHere we identify the GPR84 family of GPCRs as key regulators of effective immune cell extravasation in vivo. Mechanistically, through integrating genetically tractable Drosophila and murine in vivo models, we show how leukocyte GPR84 supports dynamic Rho-dependent detachment of stretched uropods as these cells exit vessels.

immunology↗

bioRxiv2026

Transmission strategy modulates parasite biogeography in an island-colonising bird

Parasites occur in every ecosystem, although their dispersal is often constrained by the availability of hosts or vectors. Here, we explore how variation in parasite life history traits, particularly transmission strategy, may influence their distributions. Specifically, we test whether a variety of parasites ad-here to the rules of island biogeography, and whether their distributions vary with transmission strategy. We utilised broad-spectrum parasite detection from existing Whole Genome Sequence (WGS) data to characterise parasites with varying transmission strategies from the blood of a passerine bird, the silvereye (Zosterops lateralis), sampled across 25 islands in the South Pacific and from five of the states in mainland Australia. Overall, parasite richness was higher on mainland Australia compared to islands and decreased with distance of islands from the Australian continent. However, these patterns were dependent on transmission strategy. For parasites transmitted by flying insect vectors, richness decreased on islands compared to the mainland. However, increasing isolation from the mainland among islands had little further impact. On the other hand, richness of directly transmitted parasites and those requiring another intermediate host declined sharply with increasing distance from the mainland. While islands may act as an initial barrier to colonisation for parasites relying on flying insect vectors, their highly dispersive vectors may subsequently reduce the impact of increasing isolation distance on richness. Our work underscores the importance of considering parasite life-histories and their transmission strategies for understanding the processes that shape parasite communities on islands.

ecology↗

bioRxiv2024

AI reveals a damage signalling hierarchy that coordinates different cell behaviours driving wound re-epithelialisation

One of the key tissue movements driving closure of a wound is re-epithelialisation. Earlier wound healing studies have described the dynamic cell behaviours that contribute to wound re-epithelialisation, including cell division, cell shape changes and cell migration, as well as the signals that might regulate these cell behaviours. Here, we use a series of deep learning tools to quantify the contributions of each of these cell behaviours from movies of repairing wounds in the Drosophila pupal wing epithelium. We test how each is altered following knockdown of the conserved wound repair signals, Ca2+ and JNK, as well as ablation of macrophages which supply growth factor signals believed to orchestrate aspects of the repair process. Our genetic perturbation experiments provide quantifiable insights regarding how these wound signals impact cell behaviours. We find that Ca signalling is a master regulator required for all contributing cell behaviours; JNK signalling primarily drives cell shape changes and divisions, whereas signals from macrophages regulate largely cell migration and proliferation. Our studies show AI to be a valuable tool for unravelling complex signalling hierarchies underlying tissue repair.

developmental biology↗

bioRxiv2023

Developmental mitochondrial Complex I activity determines lifespan

Aberrant mitochondrial function has been associated with an increasingly large number of human disease states. Observations from in vivo models where mitochondrial function is altered suggest that adaptations to mitochondrial dysfunction may underpin disease pathology. We hypothesized that the severity of these maladaptations could be shaped by the plasticity of the system when mitochondrial dysfunction manifests. To investigate this, we have used inducible fly models of mitochondrial complex I (CI) dysfunction to reduce mitochondrial function at two stages of the fly lifecycle, from early development and adult eclosion. Here, we show that in early life (developmental) mitochondrial dysfunction results in severe reductions in survival and stress resistance in adulthood, while flies where mitochondrial function is perturbed from adulthood, are long-lived and stress resistant despite having up to an 75% reduction in CI activity. After excluding developmental defects as a cause, we went on to molecularly characterize these two populations of mitochondrially compromised flies, short- and long-lived. We find that our short-lived flies have unique transcriptomic and metabolomic responses which overlap significantly in discreet models of CI dysfunction. Our data demonstrate that early mitochondrial dysfunction via CI depletion elicits an adaptive response which severely reduces survival, while CI depletion from adulthood is not sufficient to reduce survival and stress resistance.

molecular biology↗

bioRxiv2023

Candidate gene length polymorphisms are linked to dispersive behaviour: searching for a mechanism behind the "paradox of the great speciators"

The "paradox of the great speciators" has puzzled evolutionary biologists for over half a century. A great speciator requires excellent dispersal ability to explain its occurrence on multiple islands, but reduced dispersal ability to explain its high number of subspecies. A rapid reduction in dispersal ability is often invoked to solve this apparent paradox, but a proximate mechanism has not been identified. Here, we explore the role of six genes linked to migration and animal personality differences (CREB1, CLOCK, ADCYAP1, NPAS2, DRD4, and SERT) in 20 South Pacific populations of silvereye (Zosterops lateralis) that range from highly sedentary to partially migratory, to determine if genetic variation is associated with dispersal propensity. We detected genetic associations in three of the six genes: i) in a partial migrant population, migrant individuals had longer microsatellite alleles at the CLOCK gene compared to resident individuals from the same population; ii) CREB1 displayed longer average microsatellite allele lengths in recently colonised island populations (< 200 years), compared to evolutionarily older populations. Bayesian broken stick regression models supported a reduction in CREB1 length with time since colonisation and decreasing dispersal propensity; and iii) like CREB1, DRD4 showed differences in polymorphisms between recent and old colonisations but a further sample size is needed to confirm. ADCYAP1, SERT, and NPAS2 were variable but that variation was not associated with dispersal propensity. The association of genetic variants at three genes with migration and dispersal ability in silvereyes provides the impetus for further exploration of genetic mechanisms underlying dispersal shifts, and the prospect of resolving a long-running evolutionary paradox through a genetic lens.

evolutionary biology↗

bioRxiv2019

Syncrip/hnRNPQ is required for activity-induced Msp300/Nesprin-1 expression and new synapse formation

Memory and learning involve activity-driven expression of proteins and cytoskeletal reorganisation at new synapses, often requiring post-transcriptional regulation a long distance from corresponding nuclei. A key factor expressed early in synapse formation is Msp300/Nesprin-1, which organises actin filaments around the new synapse. How Msp300 expression is regulated during synaptic plasticity is not yet known. Here, we show that the local translation of msp300 is promoted during activity-dependent plasticity by the conserved RNA binding protein Syncrip/hnRNP Q, which binds to msp300 transcripts and is essential for plasticity. Single molecule imaging shows that Syncrip is associated in vivo with msp300 mRNA in ribosome-rich particles. Elevated neural activity alters the dynamics of Syncrip RNP granules at the synapse, suggesting a change in particle composition or binding that facilitates translation. These results introduce Syncrip as an important early-acting activity-dependent translational regulator of a plasticity gene that is strongly associated with human ataxias.\n\nSyncrip regulates synaptic plasticity via msp300Titlow et al. find that Syncrip (hnRNPQ RNA binding protein) acts directly on msp300 to modulate activity-dependent synaptic plasticity. In vivo biophysical experiments reveal activity-dependent changes in RNP complex sizes compatible with an increase in translation at the synapse.

neuroscience↗

bioRxiv2017

Regulating prospero mRNA Stability Determines When Neural Stem Cells Stop Dividing

During Drosophila and vertebrate brain development, the conserved transcription factor Prospero/Prox1 is an important regulator of the transition between proliferation and differentiation. Prospero level is low in neural stem cells and their immediate progeny, but is upregulated in larval neurons and it is unknown how this process is controlled. Here, we use single molecule fluorescent in situ hybridisation to show that larval neurons selectively transcribe a long prospero mRNA isoform containing a 15 kb 3 untranslated region, which is bound in the brain by the conserved RNA-binding protein Syncrip/hnRNPQ. Syncrip binding increases the mRNA stability of the long prospero isoform, which allows an upregulation of Prospero protein production. Our findings highlight a regulatory strategy involving alternative polyadenylation followed by differential post-transcriptional regulation.

developmental biology↗

bioRxiv2017

Lineage-specific rediploidization is a mechanism to explain time-lags between genome duplication and evolutionary diversification

The functional divergence of duplicate genes (ohnologues) retained from whole genome duplication (WGD) is thought to promote evolutionary diversification. However, species radiation and phenotypic diversification is often highly temporally-detached from WGD. Salmonid fish, whose ancestor experienced WGD by autotetraploidization ~95 Ma (i.e. Ss4R), fit such a time-lag model of post-WGD radiation, which occurred alongside a major delay in the rediploidization process. Here we propose a model called Lineage-specific Ohnologue Resolution (LORe) to address the phylogenetic and functional consequences of delayed rediploidization. Under LORe, speciation precedes rediploidization, allowing independent ohnologue divergence in sister lineages sharing an ancestral WGD event. Using cross-species sequence capture, phylogenomics and genome-wide analyses of ohnologue expression divergence, we demonstrate the major impact of LORe on salmonid evolution. One quarter of each salmonid genome, harbouring at least 4,500 ohnologues, has evolved under LORe, with rediploidization and functional divergence occurring on multiple independent occasions > 50 Myr post-WGD. We demonstrate the existence and regulatory divergence of many LORe ohnologues with functions in lineage-specific physiological adaptations that promoted salmonid species radiation. We show that LORe ohnologues are enriched for different functions than older ohnologues that began diverging in the salmonid ancestor. LORe has unappreciated significance as a nested component of post-WGD divergence that impacts the functional properties of genes, whilst providing ohnologues available solely for lineage-specific adaptation. Under LORe, which is predicted following many WGD events, the functional outcomes of WGD need not appear explosively, but can arise gradually over tens of Myr, promoting lineage-specific diversification regimes under prevailing ecological pressures.

genomics↗