Biology subjects

Schubert, N.

Publications and source records attributed to Schubert, N..

6 recordsLinked to original sources

bioRxiv2025

Crossing thermal limits: functional collapse of the surfgrass Phyllospadix scouleri under extreme marine heatwaves

Marine heatwaves (MHWs) are intensifying under climate change, yet the physiological limits that constrain seagrass resilience remain poorly defined. We experimentally tested the responses of the surfgrass Phyllospadix scouleri, a foundation species of the Northeast Pacific coast, to simulated MHWs of contrasting intensity. In a 27-day mesocosm experiment, plants were exposed to fluctuating temperatures representing a severe MHW (23.5 {+/-} 1.5 {degrees}C) and an extreme MHW (26.5 {+/-} 1.5 {degrees}C), while photosynthetic performance, respiration, nitrogen metabolism, oxidative stress, and growth were monitored during and after warming. Phyllospadix scouleri maintained photosynthetic capacity and carbon balance under severe warming but exhibited pronounced physiological disruption at extreme temperatures, including sustained photoinhibition, reduced nitrate assimilation, elevated respiration, and negative daily productivity. These effects persisted after heat stress, leading to reduced growth and indicating incomplete recovery. Multivariate analyses revealed a distinct transition from tolerance to functional breakdown near 26.5 {degrees}C, suggesting a physiological tipping point only 5-6 {degrees}C above current summer maxima in the area of the studied population. Our findings demonstrate that intensifying MHWs may rapidly erode the thermal safety margin of temperate seagrasses, pushing foundational coastal ecosystems toward metabolic instability and potential regime shifts under continued ocean warming. HighlightExtreme marine heatwave disrupts photosynthesis, nitrogen metabolism, and carbon balance in the seagrass Phyllospadix scouleri, suggesting a narrow thermal safety margin in the face of ocean warming.

plant biology↗

bioRxiv2024

Banded mongooses discriminate relatedness and MHC diversity in unfamiliar conspecifics

Olfactory cues are critical in mammalian social communication, conveying fitness-relevant information such as relatedness, genetic quality, and compatibility. Recognizing kin through scent can help avoid inbreeding depression and guide nepotistic behaviors, enhancing both direct and indirect fitness. While many species use familiarity to identify relatives, others rely on phenotype matching, where animals assess genetic similarity by comparing their own genetically determined odor with that of others. In banded mongooses, synchronized breeding disrupts familiarity cues, increasing reliance on alternative mechanisms for kin discrimination and mate selection. We tested whether banded mongooses use odors to assess genetic diversity and relatedness based on (1) major histocompatibility complex (MHC) genotypes and (2) neutral microsatellite loci that reflect genetic diversity and relatedness. We found that individuals respond differently to odors from unfamiliar individuals based on MHC diversity and genetic relatedness. Specifically, individuals show more interest in less MHC diverse and less related unfamiliar conspecifics, suggesting odor cues are used to evaluate threat level of intruders or competitors. Genetic diversity had no impact on responses to odors and was not significantly associated with MHC diversity, implying that responses to MHC diversity did not result from an underlying correlation with over-all genetic diversity. We also found no effect of MHC similarity, which might be caused by the limited sample size for this analysis. Our findings show that MHC diversity might signal the genetic quality of individuals, but regions of the genome other than MHC may be used to assess relatedness. These findings provide the basis for future research on the involvement of the MHC and other genes in social communication in species where phenotype matching is likely to be advantageous.

animal behavior and cognition↗

bioRxiv2024

Sex-dependent influence of major histocompatibility complex diversity on fitness in a social mammal

Parasite infections affect males and females differently across a wide range of species, often due to differences in immune responses. Generally, females tend to have stronger immune defenses and lower parasite loads than males. The major histocompatibility complex (MHC) plays a crucial role in the adaptive immune response, and extensive research has explored how variation in this region influences infection and fitness outcomes. However, studies of sex-specific relationships between MHC variation and infection are scarce, perhaps because MHC genes are located on the autosomes, which are shared by both sexes. Here, we provide evidence of sexually antagonistic selection in a wild, group-living mammal--the banded mongoose. Using genetic and life history data collected from over 300 individuals across 25 years, we found that particularly MHC class I (MHC-I) but also MHC class II (MHC-II) diversity influence lifetime reproductive success differently in males and females. Specifically, higher MHC diversity is linked to increased fitness in males but decreased fitness in females. Furthermore, MHC diversity did not differ between the sexes, indicating an unresolved genetic sexual conflict. Our findings demonstrate that sexually antagonistic selection acts on the MHC and may operate across both MHC classes but differently. This study contributes to the growing body of evidence that sex is a significant factor in shaping host immunity and fitness.

evolutionary biology↗

bioRxiv2024

Characterization of both major histocompatibility complex classes in a wild social mammal: the banded mongoose

The major histocompatibility complexs (MHC) role in the vertebrate adaptive immune response and its exceptional polymorphism make it a key target for studying adaptive gene evolution. However, previous studies on carnivore MHC have mostly focused on populations which experienced a severe bottleneck or are of general conservation concern. Hence, sample sizes are often small and generalizations about MHC diversity are unreliable. Furthermore, studies often focus on one MHC class and do not cover the whole peptide binding groove of the MHC molecule. Here, we characterize MHC class I (MHC-I) exon 2 and 3, encoding both the 1- and 2-domain of the MHC-I molecule, as well as MHC-II DRB exon 2 for a large sample (N = 282-485) of a wild mammal of least conservation concern, the banded mongoose. We found that MHC-I generally showed higher allelic diversity and polymorphism compared to MHC-II, which is in line with findings in humans that show higher diversifying selection acting on MHC-I. However, MHC-I exon 3 showed the lowest diversity, possibly due to its different role in generating the peptide binding groove of the class I molecule compared to exon 2. Moreover, we found selection to act more strongly on MHC-I exon 2 (domain 1) than exon 3 (domain 2). Despite frequent inbreeding, phylogenetic comparative analysis showed banded mongooses to have MHC diversity levels comparable with other carnivores of least concern. Phylogenetic analysis indicated a longer evolutionary trajectory for MHC-II compared to MHC-I as well as species-specific gene duplication of nonclassical sequences of MHC-I clustering with classical sequences. Trans-species polymorphism was detected for nonclassical MHC-I sequences suggesting homology or convergent evolution for these genes. Our study is the first to characterize both MHC classes of a social, wild carnivore using a high throughput sequencing approach with a large sample size and thereby provides the basis for further investigation of MHC structure and function within the banded mongoose and other carnivores.

genetics↗

bioRxiv2024

Selective inflammation of the tumor microenvironment and invigorated T cell-mediated tumor control upon induced systemic inactivation of TREX1

Therapeutic innate immune stimulation within the tumor microenvironment can potentiate endogenous antitumor T cell immunity. DNase 3-repair exonuclease 1 (TREX1) is essential for cellular DNA disposal which prevents autoimmunity ensuing from cGAS/STING activation by endogenous DNA. Optimal strategies to therapeutically leverage cGAS/STING signalling for cancer therapy are highly sought after. TREX1-deficient tumor cells elicit enhanced protective immunity in syngeneic models. Here we show that induced inactivation of the Trex1 gene in (non-malignant) host cells is well tolerated and yields improved type I IFN- and T cell-dependent control of established TREX1-competent tumors with selective immune cell infiltration of tumor, but not other tissues. Intra-tumoral T cell proliferation and numbers of effector and effector-like exhausted cells massively increased, enabling complete rejection in synergy with checkpoint inhibition. We conclude that systemic TREX1 inhibition is a promising approach to boost anti-tumor immunity, that can overcome immune evasion by cancer cell- intrinsic cGAS/STING inactivation.

immunology↗

bioRxiv2022

cGAS/STING-DEPENDENT SENSING OF ENDOGENOUS RNA

Defects in nucleic acid metabolizing enzymes lead to spontaneous but selective activation of either cGAS/STING or RIG-like receptor (RLR) signaling, causing a pathogenic type I interferon response and inflammatory diseases. In these pathophysiological conditions, cGAS-driven IFN production is linked to spontaneous DNA damage. Physiological, or tonic, IFN signaling on the other hand is essential to functionally prime nucleic acid sensing pathways. Here we show that low-level chronic DNA damage in mice lacking the Aicardi-Goutieres syndrome gene SAMHD1 reduced tumor-free survival when crossed to a p53-deficient, but not to DNA mismatch repair-deficient background. Increased DNA damage did not result in higher levels of type I interferon. Instead, we found that the chronic interferon response in SAMHD1-deficient mice was driven by the MDA5/MAVS pathway but required functional priming through the cGAS/STING pathway. Our work positions cGAS/STING upstream of tonic IFN signaling and highlights an important role of the pathway in physiological and pathophysiological innate immune priming. SummaryLoss of the dNTPase and DNA repair enzyme SAMHD1 is associated with cancer and causes systemic autoimmunity. We show transformation-promoting spontaneous DNA damage and MDA5-driven but cGAS/STING-dependent chronic type I interferon production in SAMHD1-deficient mice.

immunology↗