Biology subjects

Hays, C.

Publications and source records attributed to Hays, C..

5 recordsLinked to original sources

bioRxiv2026

A mosaic of climate vulnerability: local warming rates meet intraspecific divergence in heat tolerance

Climate warming is increasing mismatches between thermal phenotypes and habitat temperatures, driving range shifts and population extirpations. While within-species variation in heat tolerance and local warming rates can predict responses to climate warming, how these factors shape differences in vulnerability among taxa and ecosystems is uncertain. Here we combine climate and thermal trait data from 69 species across four ecosystem types to examine the effects of incorporating intraspecific variation in heat tolerance and local warming rates on projected vulnerability to climate warming. Because vulnerability to warming depends on existing phenotypic variation in thermal performance and relative rates of habitat warming, we develop a new metric that integrates localized rates of warming with spatial variation in thermal tolerances, termed the minimum trait velocity. Incorporating intraspecific variation in heat tolerance lowered estimates of warming tolerance (a measure of vulnerability) across most ecosystem types, with the strongest negative impact on marine taxa. Although intraspecific variation in heat tolerance could facilitate adaptation to climate change, our results suggest such variation is generally less than the projected near future warming. This suggests that opportunities for evolutionary rescue via gene flow between locally adapted populations are limited, adding to mounting concern as the climate warms.

ecology↗

bioRxiv2025

Targeted RNAi screen reveals novel regulators of RNA-binding protein phase transitions in Caenorhabditis elegans oocytes

The ability of oocytes to maintain their quality is essential for successful reproduction. One critical aspect of oocyte quality and successful embryogenesis after fertilization is the proper regulation of the stores of maternal mRNA by RNA-binding proteins. Many RNA-binding proteins undergo regulated phase transitions during oogenesis, and alterations of the protein phase can disrupt its ability to regulate mRNA stability and translation. In C. elegans, genetic screens have identified regulators of RNA-binding protein condensation in arrested oocytes of females and in embryos, but less attention has focused on phase transitions in maturing oocytes of young adult hermaphrodites. Interestingly, of the relatively few regulators of RNA-binding protein phase transitions identified to date in maturing oocytes, several genes overlap with those required for clearance of protein aggregates in maturing oocytes. To determine the extent to which the temporally linked processes of clearance of damaged proteins and maintenance of RNP complexes are coordinated at a molecular level, we conducted a targeted RNAi screen of genes required for removal of protein aggregates in maturing oocytes. We identified six novel regulators of phase transitions of the KH-domain protein MEX-3 and obtained strong evidence that the regulatory network of protein aggregate clearance overlaps with, but is distinct from, the regulation of MEX-3 phase transitions in the oocyte.

genetics↗

bioRxiv2025

Monitoring the stability of transgene expression in lettuce using the RUBY reporter.

Nearly four decades after the first transgenic lettuce was reported, constructs for stable transgene expression remain limited. Notably, the 35S promoter from the Cauliflower Mosaic Virus (35S), which drives strong expression of transgenes in several plant species, has often shown silencing and instability in lettuce. Other promoter/terminator combinations that are commonly used in plant expression vectors have not been extensively studied in lettuce. In this study, we evaluated three different expression constructs in two different horticultural types of lettuce using the non-invasive RUBY reporter, which allowed for the monitoring of transgene expression throughout the process of regeneration during tissue culture, throughout development of the primary transgenics, and in two subsequent sexual generations. The LsUBI promoter/terminator combination resulted in strong, uniform expression throughout regeneration, during growth of the primary transgenics, and in both subsequent generations. The AtUBI promoter/tRBCS combination showed slightly lower levels of expression and intermediate levels of silencing, while the 35S promoter/tHSP combination showed both initial strong expression and frequent silencing. Therefore, our data show that the LsUBI promoter/terminator combination provides strong, uniform expression that is unlikely to result in silencing and that the AtUBI promoter/tRBCS combination is an additional option for stable expression of transgenes in lettuce, especially if an intermediate expression level is desired.

plant biology↗

bioRxiv2022

Specific interaction between Group B Streptococcus CC17 hypervirulent clone and phagocytes

Streptococcus agalactiae also named Group B Streptococcus (GBS) is the most significant pathogen causing invasive infections, such as bacteremia and meningitis, in neonates. Worldwide epidemiological studies have shown that a particular clonal complex (CC) of capsular serotype III, the CC17, is strongly associated with meningitis in neonates and is therefore designated as the hypervirulent clone. Macrophages are a permissive niche for intracellular bacteria of all GBS clones. In this study we deciphered the specific interaction of GBS CC17 strains with macrophages. Our study revealed that CC17 strains are phagocytosed at a higher rate than GBS non-CC17 strains by human monocytes and macrophages both in cellular models and primary cells. CC17 enhanced phagocytosis is due to an initial enhanced-attachment step to macrophages mediated by the CC17 specific surface protein HvgA and the PI-2b pilus (Spb1). We showed that two different inhibitors of scavenger receptors (fucoidan and poly(I)) specifically inhibited CC17 adhesion and phagocytosis while not affecting those of non-CC17 strains. Once phagocytosed, both CC17 and non-CC17 strains remained in a LAMP-1 positive vacuole that ultimately fuses with lysosomes where they can survive at similar rates. Finally, both strains displayed a basal egress which occurs independently from actin and microtubule networks. Our findings provide new insights into the interplay between the hypervirulent GBS CC17 and major players of the hosts innate immune response. This enhanced adhesion leading to higher phagocytosis could reflect a peculiar capacity of the CC17 lineage to subvert the host immune defenses, establish a niche for persistence or disseminate.

microbiology↗

bioRxiv2021

Convergence of case-specific epigenetic alterations identify a confluence of genetic vulnerabilities tied to opioid dependence

Opioid dependence is a highly heterogeneous disease driven by a variety of genetic and environmental risk factors which have yet to be fully elucidated. We interrogated the effects of opioid dependence on the brain using ChIP-seq to quantify patterns of H3K27 acetylation in dorsolateral prefrontal cortical neurons isolated from 51 opioid-overdose cases and 51 accidental death controls. Among opioid cases, we observed global hypoacetylation and identified 388 putative enhancers consistently depleted for H3K27ac. Machine learning on H3K27ac patterns predicts case-control status with high accuracy. We focus on case-specific regulatory alterations, revealing 81,399 hypoacetylation events, uncovering vast inter-patient heterogeneity. We developed a strategy to decode this heterogeneity based on convergence analysis, which leveraged promoter-capture Hi-C to identify five genes over-burdened by alterations in their regulatory network or "plexus": ASTN2, KCNMA1, DUSP4, GABBR2, ENOX1. These convergent loci are enriched for opioid use disorder risk genes and heritability for generalized anxiety, number of sexual partners, and years of education. Overall, our multi-pronged approach uncovers neurobiological aspects of opioid dependence and captures genetic and environmental factors perpetuating the opioid epidemic.

genomics↗