Biology subjects

Barton, H. J.

Publications and source records attributed to Barton, H. J..

4 recordsLinked to original sources

bioRxiv2026

Microspatial partitioning of insect-specific viromes and dengue virus transmission risk by Aedes aegypti in Puerto Rico

Mosquito-borne arboviruses remain a major global health threat. Although insect-specific viruses (ISVs) may influence arbovirus transmission across geographic regions, their diversity within Aedes aegypti populations at microspatial scales remains poorly understood. We hypothesized that local environmental variation shapes the A. aegypti core virome, producing distinct ISV profiles in rural and urban populations in Puerto Rico. Metatranscriptomic RNA sequencing of F0 mosquitoes identified thirteen ISVs with habitat-specific virome composition. Partitiviridae was the dominant viral family, while Humaita-Tubiacanga virus (HTV) and Phasi Charoen-like phasivirus (PCLV) exhibited the highest abundance, persistence, and prevalence in urban laboratory colonies. Urban A. aegypti also showed significantly higher dengue virus-1 (DENV-1) infection rates than rural populations, although saliva positivity remained low and did not differ significantly between the two groups. These findings indicate that microspatial ecological variation shapes the A. aegypti virome, but the association of HTV/PCLV with DENV-1 transmission risk is likely multifactorial and nuanced.

microbiology↗

bioRxiv2026

Dfm1 promotes Ste24-dependent translocon quality control

Proteins stalled during endoplasmic reticulum translocation clog Sec61 channels and require translocon quality control (TQC) mechanisms for clearance. Genetic screens implicated the derlin Dfm1 in TQC; however, its mechanistic role remained unclear. Using engineered and disease-relevant translocon-clogging substrates in Saccharomyces cerevisiae, we show Dfm1 functions in the Ste24-dependent branch of TQC, but not Hrd1- or Ltn1-dependent pathways. Loss of DFM1 increased accumulation and toxicity of translocon-clogging proteins. Increased dosage of wild type or catalytically inactive Hrd1 or Ste24 rescued toxicity, supporting a non-enzymatic buffering function for these factors in TQC. These findings identify Dfm1 as a key TQC factor whose critical role in clearing clogged translocons can be suppressed in multiple ways. Our results suggest enhancing TQC may protect cells from proteotoxic stress caused by disease-relevant translocon-clogging substrates, with potential implications for pancreatic {beta}-cell dysfunction in diabetes. Significance StatementO_LICells rely on translocon quality control (TQC) to clear proteins that clog the Sec61 translocon, but how the derlin Dfm1 contributes to this process has remained unclear. C_LIO_LIWe demonstrate that Dfm1 functions specifically in the Ste24-dependent TQC pathway and show that increased levels of the TQC factors Hrd1 or Ste24 rescues Dfm1 deficiency even without catalytic activity, revealing an unexpected non-enzymatic buffering function. C_LIO_LIThis work defines Dfm1s mechanistic role in TQC, provides new insight into how cells preserve endoplasmic reticulum function during translocation stress, and establishes a framework for investigating conserved pathways that protect against diseases associated with translocon clogging. C_LI

cell biology↗

bioRxiv2021

The effective population size modulates the strength of GC biased gene conversion in two passerines

Understanding the determinants of genomic base composition is fundamental to understanding genome evolution. GC biased gene conversion (gBGC) is a key driving force behind genomic GC content, through the preferential incorporation of GC alleles over AT alleles during recombination, driving them towards fixation. The majority of work on gBGC has focussed on its role in coding regions, largely to address how it confounds estimates of selection. Non-coding regions have received less attention, particularly in regard to the interaction of gBGC and the effective population size (Ne) within and between species. To address this, we investigate how the strength of gBGC (B = 4Neb, where b is the conversion bias) varies within the non-coding genome of two wild passerines. We use a dataset of published high coverage genomes (10 great tits and 10 zebra finches) to estimate B, nucleotide diversity, changes in Ne, and crossover rates from linkage maps, in 1Mb homologous windows in each species. We demonstrate remarkable conservation of both B and crossover rate between species. We show that the mean strength of gBGC in the zebra finch is more than double that in the great tit, consistent with its twofold greater effective population size. B also correlates with both crossover rate and nucleotide diversity in each species. Finally, we estimate equilibrium GC content from both divergence and polymorphism data, which indicates that B has been increasing in both species, and provide support for population expansion explaining a large proportion of this increase in the zebra finch. Significance statementUnderstanding the forces that change the nucleotide base composition of genomes is central to understanding their evolution. One such force is GC biased gene conversion, a process that during recombination converts some heterozygous base positions to homozygous. This process is more likely to convert adenine and thymine bases to guanine and cytosine bases than the other way around, hence is GC biased. This increases the frequency of GC alleles in a way similar to positive selection. This process has largely been studied within protein coding regions, and not often compared between species. We measure its strength in the non-coding areas of the genomes of two bird species, showing it to be stronger in the species with the larger population size.

genetics↗

bioRxiv2019

Non-coding rather than coding regions underpin avian bill shape diversification at macroevolutionary scales

Recent progress has been made in identifying genomic regions implicated in trait evolution on a microevolutionary scale in many species, but whether these are relevant over macroevolutionary time remains unclear. Here, we directly address this fundamental question using bird beak shape, a key evolutionary innovation linked to patterns of resource use, divergence and speciation, as a model trait. We integrate class-wide geometric-morphometric analyses with evolutionary sequence analyses of 10,322 protein coding genes as well as 229,001 genomic regions spanning 72 species. We identify 1,434 protein coding genes and 39,806 noncoding regions for which molecular rates were significantly related to rates of bill shape evolution. We show that homologs of the identified protein coding genes as well as genes in close proximity to the identified noncoding regions are involved in craniofacial embryo development in mammals. They are associated with embryonic stem cells pathways, including BMP and Wnt signalling, both of which have repeatedly been implicated in the morphological development of avian beaks. This suggests that identifying genotype-phenotype association on a genome wide scale over macroevolutionary time is feasible. While the coding and noncoding gene sets are associated with similar pathways, the actual genes are highly distinct, with significantly reduced overlap between them and bill-related phenotype associations specific to noncoding loci. Evidence for signatures of recent diversifying selection on our identified noncoding loci in Darwin finch populations further suggests that regulatory rather than coding changes are major drivers of morphological diversification over macroevolutionary times.

evolutionary biology↗