Biology subjects

Robinson, J. D.

Publications and source records attributed to Robinson, J. D..

4 recordsLinked to original sources

bioRxiv2026

Warm temperature impedes the spread of a heritable manipulative symbiont community in spider populations

Heritable bacterial symbionts are pervasive in terrestrial arthropods, often imposing reproductive manipulations to promote their own spread within host populations. Co-infections are common, potentially allowing symbiont co-infectors to hitchhike through a host population. However, adverse thermal conditions can disrupt these communities, particularly when co-infectors vary in their thermal sensitivity. We used a multi-generation experiment to test whether warm (29 {degrees}C) conditions disrupted spread of heritable symbionts through uninfected populations of the spider, Mermessus fradeorum. We tested two common infection combinations: a single infection with a cytoplasmic incompatibility (CI) inducing Rickettsiella or a feminizing co-infection that included a feminizing Wolbachia, the same Rickettsiella, and up to three apparent hitchhikers (two additional Wolbachia strains and Tisiphia). We initiated replicate populations with 1/3 of one infection type and 2/3 uninfected spiders, evaluating population infection rate over 5 spider generations under different temperature regimes. Under cool (21{degrees}C) conditions, Wolbachia feminization drove co-infection to 88% and Rickettsiella CI drove single infection to 83% of host populations. Vertical transmission for all symbionts was high (97-99%) and hitchhiking symbionts also spread effectively. Under warm conditions, feminization and CI efficacy were reduced, and symbionts suffered variably reduced vertical transmission. Warm conditions ultimately destroyed the co-infecting symbiont consortium and impeded symbiont spread. On its own, though, Rickettsiella was still able to increase, despite reduced strength of CI. We hypothesize that contrasting tensions between feminizing spread of the symbiont consortium versus environmentally driven loss of function and transmission may explain observed patterns of mixed infections in field populations of this spider.

ecology↗

bioRxiv2026

Emotion regulation or dual task? Dissociation of neural and behavioral measures

Cognitive reappraisal, the deliberate reinterpretation of emotional events, is widely considered an effective emotion regulation strategy, and modulation of the late positive potential (LPP) during negative affect reduction has become the primary electrophysiological evidence for volitional emotional control. Experimental instructions, however, impose dual-task demands that free viewing does not, confounding reappraisal with cognitive load. By including instructions to increase emotional responses to pictures ("enhance") as well as instructions to decrease ("suppress"), different predictions are generated. If the LPP reflects regulation, then, compared to free viewing, suppress instructions should decrease LPP amplitude, and enhance instructions should increase LPP amplitude. If modulation instead reflects cognitive load, both instructions should reduce the LPP, as both impose an additional cognitive task. In a sample of 107 participants, evaluative ratings confirmed that regulation instructions modulated reported emotional intensity in the expected directions (Enhance > View > Suppress), but that both enhance and suppress instructions reduced LPP amplitude compared to free viewing, with Bayesian model comparisons providing strong evidence against direction-specific regulation and in favor of cognitive load. Whole-scalp multivariate pattern analysis confirmed that no instruction-related neural signal exists at any scalp location or latency within the first second after stimulus onset. These data indicate that LPP modulation following both instruction types reflects dual-task cognitive load rather than volitional emotional control. Significance StatementCognitive reappraisal is considered the gold standard of emotion regulation, and reduced late positive potential (LPP) amplitude during negative emotion suppression is the primary neural evidence that humans can voluntarily control emotional responses. The current data are inconsistent with this regulatory account and instead support a cognitive load interpretation. Whether instructed to enhance or suppress emotional responses, LPP amplitude was reduced in both conditions relative to free viewing, consistent with attentional resource competition rather than directional regulatory control. The same participants reported successfully regulating emotional experience in opposite directions, producing a clear dissociation between neural and behavioral measures. These findings challenge a basic tenet of emotional regulation and raise questions concerning LPP modulation as a biomarker of regulatory capacity.

neuroscience↗

bioRxiv2022

NMY-2, TOE-2 and PIG-1 Regulate C. elegans Asymmetric Cell Divisions

Asymmetric cell division (ACD) is an important mechanism that generates cellular diversity during development. Not only do asymmetric cell divisions produce daughter cells of different fates, many can produce daughters of different sizes, which we refer to as Daughter Cell Size Asymmetry (DCSA). In C. elegans, apoptotic cells are frequently produced by asymmetric divisions that exhibit DCSA, where the smaller daughter dies. We focus here on the divisions of the Q.a and Q.p neuroblasts, which produce apoptotic cells and divide with opposite polarity using both distinct and overlapping mechanisms. The PIG-1/MELK and TOE-2 proteins both regulate DCSA and specify the apoptotic cell fate in both the Q.a and Q.p divisions. In many asymmetric cell divisions, the non-muscle myosin NMY-2 is involved in properly positioning the cleavage furrow to produce daughters of unequal size. It was previously reported that NMY-2 is asymmetrically distributed and required for the DCSA of Q.a but not Q.p. In this study, we examined endogenously tagged reporters of NMY-2, TOE-2, and PIG-1 and found that all were asymmetric at the cortex during both the Q.a and Q.p divisions. TOE-2 and NMY-2 were biased toward the side of the dividing cell that would produce the smaller daughter, whereas PIG-1 was biased toward the side that would produce the larger daughter. We used temperature-sensitive nmy-2 mutants to determine the role of nmy-2 in these divisions and found that these mutants only displayed DCSA defects in the Q.p division. We generated double mutant combinations between the nmy-2 mutations and mutations in toe-2 and pig-1. The nmy-2 mutations did not significantly alter the DCSA of the toe-2 and pig-1 mutants but did alter the fate of the Q.a and Q.p daughters. This finding suggests that NMY-2 functions together with TOE-2 and PIG-1 to regulate DCSA but plays an independent role in specifying the fate of the Q.a and Q.p descendants.

genetics↗

bioRxiv2021

Differential gene expression reveals host factors for viral shedding variation in mallards (Anas platyrhynchos) infected with low-pathogenic avian influenza virus

Intraspecific variation in pathogen shedding impacts disease transmission dynamics; therefore, understanding the host factors associated with individual variation in pathogen shedding is key to controlling and preventing outbreaks. In this study, ileum and bursa of Fabricius tissues of mallards (Anas platyrhynchos) infected with low-pathogenic avian influenza (LPAIV) were evaluated at various post-infection time points to determine genetic host factors associated with intraspecific variation in viral shedding. By analyzing transcriptome sequencing data (RNA-seq), we found that LPAIV-infected mallards do not exhibit differential gene expression compared to uninfected birds, but that gene expression was associated with viral shedding quantity early in the infection. In both tissues, immune genes were mostly up-regulated in higher shedding birds and had significant positive relationships with viral shedding. In the ileum, host genes involved in viral cell entry were down-regulated in low shedders one day post-infection (DPI), and host genes promoting viral replication were up-regulated in high shedders on two DPI. Our findings indicate that viral shedding is a key factor for gene expression differences in LPAIV-infected mallards, and the genes identified in this study could be important for understanding the molecular mechanisms driving intraspecific variation in pathogen shedding.

genomics↗