Biology subjects

Hayward, L.

Publications and source records attributed to Hayward, L..

3 recordsLinked to original sources

bioRxiv2026

Novel but stable endosymbionts have contrasting effects on aphid dispersal and plant feeding damage in the cereal pest Diuraphis noxia

Endosymbiotic bacteria can affect many ecological attributes of their insect hosts, including (in herbivorous insects) how insects interact with plants where they feed. This raises the issue of whether deliberate endosymbiont introductions could be used to decrease crop damage caused by insect pests. Here we investigate how transinfecting Rickettsiella viridis and Regiella insecticola endosymbionts into a novel pest aphid host, the Russian wheat aphid (Diuraphis noxia), influences population growth, alate production, dispersal ability and crop damage. Both the Rickettsiella (originating from pea aphids) and Regiella (from green peach aphids) were stably maintained in their new host where they had contrasting effects. Rickettsiella increased the severity of aphid damage on wheat and barley, resulting in greater leaf loss, chlorotic streaking, and higher aphid populations, whereas Regiella reduced aphid population growth and the severity of feeding damage by aphids. Their effects on dispersal morphology also differed: Regiella had no detectable impact on alate incidence, while Rickettsiella consistently suppressed wing formation in small cages, and in larger mesocosms with multiple wheat plants this endosymbiont suppressed dispersal. Endosymbiont-mediated changes in feeding damage did not involve the main plant immune response pathways: transinfected and wild type aphids induced similar levels of jasmonic acid, jasmonic acid-isoleucine, and salicylic acid in plant tissues, even though these plant defenses were strongly activated during aphid feeding. Novel endosymbionts can therefore modulate the severity of plant feeding damage by aphids as well as influencing aphid dispersal. Potential applications in controlling pest D. noxia populations are discussed. Significance statementEndosymbiotic bacteria that live within insect cells can have wide-ranging effects on the reproduction and fitness of their insect hosts in different environments. In herbivorous insects this includes effects on host plant use. Here we test if novel endosymbionts in a pest aphid, the Russian wheat aphid, might be used to decrease crop damage and dispersal. We show that the damage caused to wheat and barley plants from aphid feeding is modulated by novel but stably transmitted introduced endosymbionts. One endosymbiont (Rickettsiella) increased the severity of damage but decreased aphid dispersal, while another (Regiella) decreased damage severity without impacting dispersal. These contrasting effects may be associated with changes in aphid population growth and wing formation but were not linked to key plant immune response pathways. We discuss implications of these findings for using endosymbionts in agricultural pest management. Classification: Applied Biological Sciences, microbiology

microbiology↗

bioRxiv2025

Spiroplasma and heat hardening can buffer insect male fertility loss at high temperatures

Insects upper thermal limits for survival, activity, and fertility have been used to assess vulnerability to climate change, yet heritable endosymbionts - present in over 70% of insect species - are often overlooked. While emerging research suggests some endosymbionts can increase thermal tolerance, their effects on upper lethal and fertility thermal limits has rarely been investigated. Additionally, short-term exposure to sub-lethal high temperatures (heat hardening) can increase insect heat tolerance, but its impact on male fertility is unclear and potential interactions with endosymbionts has not been explored. Here, we investigate whether the endosymbiont Spiroplasma poulsonii and heat hardening influence upper survival and fertility thermal limits in a native widespread host of Spiroplasma (Drosophila hydei) and a novel host (Drosophila birchii), a rainforest-restricted species with low heat tolerance. Heat hardening generally improved survival and fertility following a heat shock. The presence of Spiroplasma increased survival and fertility of D. hydei males following heat-shock, while in D. birchii, it did not enhance survival but protected male fertility after heat-shock and modulated hardening responses at sub-lethal temperatures. While protective effects varied across species, sex, and trait, both Spiroplasma and hardening significantly buffered male fitness loss during heat shock in both host species and halved heat exposure risk under current and predicted climate change in the rainforest restricted D. birchii. These findings highlight that, beyond generating novel phenotypic variation, endosymbionts can interact with plastic responses to heat stress, emphasising the importance of accounting for endosymbiont-mediated effects on thermal tolerance when assessing insect vulnerability to climate change and exploring strategies to manipulate insect thermal tolerance.

evolutionary biology↗

bioRxiv2025

Mutation-selection-drift balance models of complex diseases

Genetic variation that influences complex disease susceptibility is introduced into the population by mutation and removed by natural selection and genetic drift. This mutation-selection-drift-balance (MSDB) shapes the prevalence of a disease and its genetic architecture. To date, however, MSDB has only been modeled for monogenic (Mendelian) diseases. Here, we develop a MSDB model for complex disease susceptibility: we assume that genotype relates to disease risk according to the canonical liability threshold model and that selection on variants affecting risk derives from the fitness cost of the disease, and focus on diseases that are highly polygenic, entail a substantial fitness cost, and are neither extremely common in the population nor exceedingly rare. Contrasting model predictions with GWAS and other findings in humans suggests that directional selection plays little role in shaping common genetic variation affecting complex disease susceptibility but might substantially affect rare, large effect variation. In turn, common variation affecting complex disease susceptibility appears to be dominated by pleiotropic stabilizing selection on other traits. Our results further suggest that current estimates of disease heritability are likely biased. More generally, our model provides a better understanding of the evolutionary processes that shape the architecture and prevalence of complex diseases.

genetics↗