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Biology subjects

Han, Z.-Y.

Publications and source records attributed to Han, Z.-Y..

9 recordsLinked to original sources

Scaling temperature-dependent dispersal rates to metacommunity dynamics: An experimental test

O_LIChanges in community structure under shifting thermal regimes depend on how both local population dynamics and regional dispersal respond to temperature. Processes underlying dispersal, such as movement speed and density dependence, are constrained by temperature-dependent metabolic rates; however, the temperature dependence of population dispersal rate, and effect of this relationship on local and regional diversity patterns, have received little attention in the metabolic scaling literature. C_LIO_LIHere, we propose and experimentally test a framework that relates temperature effects on individual dispersal probability, to thermal performance curves (TPCs) for population dispersal rates, to colonization dynamics in metacommunities. Using multi-patch well plate microcosms, we measured thermal performance curves for dispersal rate in several naturally co-occurring ciliate species, and contrasted species-specific dispersal TPCs at different intra- and inter-specific densities and time scales. C_LIO_LIDispersal rate TPCs in monoculture differed at low versus high population densities, potentially suggesting distinct temperature effects on the density-independent (individual movement probability and speed) and density-dependent (quorum-sensing and resource competition) components of dispersal. C_LIO_LISpecies-specific dispersal rate TPCs in polyculture metacommunities explained differences in colonization dynamics across temperature treatments. Dispersal rate TPCs differed from intrinsic growth rate TPCs, such that better dispersers had higher-than-expected per capita population growth at the regional (whole-metacommunity) scale compared to predictions from standard growth TPCs measured in single-patch monoculture. C_LIO_LITogether, these results suggest that ignoring temperature-dependent dispersal can yield an incomplete understanding of biodiversity change in spatially structured systems exposed to warming. C_LI

ecology↗

Ecological interactions mediate evolutionary responses to temperature in microbial communities

Microbial populations play a pivotal role in ecosystem-level responses to rising temperatures and both their ecology and evolution can be directly influenced by warming. However, predicting microbial evolution and its ecological consequences is challenging because different genotypes within a population might respond uniquely to shifts in the abiotic and biotic environment. To understand how, we quantified evolutionary and ecological responses across temperatures in a protist of wide geographic distribution in the presence and absence of other microbial species with whom they interact (i.e., heterospecifics). In the absence of heterospecifics, we found that intraspecific interactions and warming selected in favor of a particular genotype, reducing genotypic diversity. In the presence of heterospecifics, 1) genetic diversity was further reduced under warming, resulting in temperature-dependent selection; but, 2) the magnitude of this change depended on the sign (+, 0, -) of the net ecological effect on the focal species by the heterospecifics, and this effect was itself temperature-dependent. Together, our results demonstrate that both intra- and interspecific interactions can mediate how temperature shapes microbial population rapid evolutionary responses, underscoring the importance of the ecological context in predicting evolutionary outcomes under climate change.

ecology↗

Myeloid reprogramming by poly(I:C) recruits progenitor-exhausted CD8+ T cells and sensitizes rhabdoid tumors to PD-1 blockade

Immune exclusion remains a major barrier to effective immunotherapy in solid tumors. Given the abundance and plasticity of tumor-associated macrophages (TAMs) in many tumors, including pediatric tumors, we investigated whether TLR3 activation could reprogram them to facilitate immune access. Single-cell and spatial profiling in a mouse model of rhabdoid tumors showed that they are dominated by TLR3-expressing TAMs, whose depletion delays tumor growth. Treatment with the TLR3 agonist poly(I:C) promotes immune cell infiltration, including progenitor-exhausted CD8+ T cells, by multiple mechanisms including the reduction and reprogramming of immunosuppressive TAMs, promoting nitric-oxide production by peritumoral macrophages, and inducing CXCL9/10 production. Combined poly(I:C) and PD-1 blockade elicited durable, complete tumor rejection. Human macrophages from tumor biopsies showed conserved TLR3 responsiveness, underscoring translational potential. These findings uncover a mechanism by which TLR3-driven myeloid reprogramming transforms immune-excluded tumors into checkpoint-responsive ones, revealing a therapeutic path to overcome resistance to PD-1 blockade.

immunology↗

Dual PD-L1/TIGIT blockade induces PNAd+ HEV-like vessels and CD62L+ lymphocyte recruitment, driving rhabdoid tumor rejection

Rhabdoid tumors (RTs) are aggressive pediatric malignancies with poor prognosis and limited immunotherapy options. Here, we investigate the therapeutic potential of combined PD-L1 (Programmed cell death ligand 1) and TIGIT (T cell immunoreceptor with Ig and ITIM domains) immune checkpoint blockade in RTs using a preclinical murine model that recapitulates key features of human ATRT (Atypical teratoid rhabdoid tumors) subtypes. Transcriptomic analyses of human and murine RTs reveal co-expression of TIGIT and PD-1 (Programmed cell death 1) pathway components and their ligands, particularly in immune-infiltrated subtypes, supporting a rationale for dual blockade. Combination therapy induces complete tumor regression, prolongs survival, and reprograms the tumor immune microenvironment by enriching CD62L naive and central memory T cells and promoting selective T-cell clonal expansion. Notably, dual blockade initiates PNAd (Peripheral node addressin) high endothelial venule (HEV)-like structures, associated with focal lymphocyte clustering and enhanced immune cell recruitment. These findings reveal a mechanistic link between vascular remodeling and immune infiltration and support dual TIGIT and PD-L1 inhibition as a promising immunotherapeutic strategy for RTs.

immunology↗

Species interactions and food-web context drive temperature-dependent prey evolution

Global warming is reshaping food webs globally. Rapid evolution has been proposed as a buffer against climate change, but how simultaneous shifts in biotic and abiotic environments may influence evolution is unknown. Using experimental evolution and mathematical modeling in microbial food webs of prey algae and ciliate predators, we tested 1) how temperature affects prey evolution and 2) how the food-web context--i.e., predator identity, abundance, and competition among predators-- mediates prey evolutionary dynamics. We found that temperature alone does not drive prey evolution unless predators are present, and food-web context determines ensuing evolutionary dynamics. These seemingly complex evolutionary responses are predictable from the joint effects of temperature-dependent, predator-specific predation rates, and the emergence of temperature-dependent prey plasticity. We reveal that evolutionary outcomes under warming are shaped by the broader food web context of species, suggesting that the same species may exhibit different eco-evolutionary responses in different food webs under novel climates. SIGNIFICANCEPredicting how species evolve under climate change is critical for understanding future changes in food webs. Evolutionary responses have long been known to be driven by environmental change--like temperature--but whether and how ecological interactions influence this process is unknown. Using experimental evolution and mathematical modeling, we show that temperature alone does not drive prey evolution. Instead, the broader food webs context--predator identity, abundance, and competition--mediates how species evolve under warming. Additionally, we demonstrate that prey evolution depends on temperature-dependent predator-specific predation rates and prey plasticity. Our findings highlight that the same species may evolve differently within different food webs, urging the need to integrate ecological interactions when forecasting evolutionary responses to climate change.

ecology↗

Rapid adaptive evolution of microbial thermal performance curves

Microbial respiration is a key biotic driver of climate change. Warming boosts microbial population growth, which increases biomass and respiration. This feedback might be disrupted by adaptation in thermal performance curves (TPCs) -whose shape describes how temperature drives growth. In this study, we uncover substantial genetic variation (G) in microbial intrinsic population growth rates (r), demonstrate a causal link between G variation in r and G variation in TPC shape, and show how this variation constrains r-TPC shape evolution along specific evolutionary paths across temperatures. We also uncover Gene-by-Environment (G x E) variation in r, which results in specific signatures in TPC shape and predictable temperature-dependent rapid TPC evolution but also lower G, which could reduce future evolutionary potential. Overall, we show how temperature-dependent evolution in a linchpin of global ecosystem function--microbial TPC shape--is determined by a combination of heritable and non-heritable variation in intrinsic growth rates.

ecology↗

Rapid eco-phenotypic feedbacks and the temperature response of biomass dynamics

As biomass dynamics capture information on population dynamics and ecosystem-level processes (e.g., changes in production over time), understanding how rising temperatures associated with global climate change influence biomass dynamics is a pressing issue in ecology. The total biomass of a species depends on its density and its average mass. Disentangling how biomass dynamics may respond to increasingly warm and variable temperatures may thus ultimately depend on understanding how temperature influences both density and mass dynamics. Here, we address this issue by keeping track of experimental microbial populations growing to carrying capacity for 15 days at two different temperatures in the presence and absence of temperature variability. We show that temperature influences biomass through its effects on density and mass dynamics, which have opposite effects on biomass and can offset each other. We also show that temperature variability influences biomass, but that effect is independent of any effects on density or mass dynamics. Last, we show that reciprocal effects of density and mass shift significantly across temperature regimes, suggesting that rapid and environment-dependent eco-phenotypic dynamics underlie biomass responses. Overall, our results connect temperature effects on population and phenotypic dynamics to explain how biomass responds to temperature regimes, thus shedding light on processes at play in cosmopolitan and massively abundant microbes as the world experiences increasingly hot and variable temperatures.

ecology↗

Temperature and nutrients drive complex eco-phenotypic dynamics in a microbial food web

Anthropogenic increases in temperature and nutrient loads will likely impact food web structure and stability. Although their independent effects have been reasonably well studied, their joint effects--particularly on coupled ecological and phenotypic dynamics--remain poorly understood. Here we experimentally manipulated temperature and nutrient levels in microbial food webs and used time-series analysis to quantify the strength of reciprocal effects between ecological and phenotypic dynamics across trophic levels. We found that i) joint -often interactive- effects of temperature and nutrients on ecological dynamics are more common at higher trophic levels, ii) temperature and nutrients interact to shift the relative strength of top-down vs. bottom-up control, and iii) rapid phenotypic change mediates observed ecological responses to changes in temperature and nutrients. Our results uncover how feedbacks between ecological and phenotypic dynamics mediate food web responses to environmental change. This suggests important but previously unknown ways that temperature and nutrients might jointly control the rapid eco-phenotypic feedbacks that determine food web dynamics in a changing world.

ecology↗

Rapid plastic shifts in body size precede and determine population growth

O_LIBody size is a fundamental trait linked to many ecological processes--from individuals to ecosystems. Although the effects of body size on metabolism are well-known, the potential reciprocal effects of body size and density are less clear. Specifically, 1) whether changes in body size or density more strongly influence the other and 2) whether coupled rapid changes in body size and density are due to plasticity, rapid evolutionary change, or a combination of both. C_LIO_LIHere, we address these two issues by experimentally tracking population density and mean body size in the protist Tetrahymena pyriformis as it grows from low density to carrying capacity. We then use Convergent Cross Mapping time series analyses to infer the direction, magnitude, and causality of the link between body size and ecological dynamics. We confirm the results of our analysis by experimentally manipulating body size and density while keeping the other constant. Last, we fit mathematical models to our experimental time series that account for purely plastic change in body size, rapid evolution in size, or a combination of both, to gain insight into the processes that most likely explain the observed dynamics. C_LIO_LIOur results indicate that changes in body size more strongly influence changes in density than the other way around, but also show that there is reciprocity in this effect (i.e., a feedback). We show that a model that only accounts for purely plastic change in size most parsimoniously explains observed, coupled phenotypic and ecological dynamics. C_LIO_LITogether, these results suggest 1) that body size can shift dramatically through plasticity, well within ecological timescales, 2) that rapid changes in body size may have a larger effect on ecological dynamics than the reverse, but 3) phenotypic and ecological dynamics influence each as populations grow. Overall, we show that rapid plastic changes in functional traits like body size may play a fundamental -but currently unrecognized- role in familiar ecological processes such as logistic population growth. C_LI

ecology↗