Rapid climate change at the end of the Permian Period (~252 million years ago) is the hypothesized trigger for the largest mass extinction in Earth’s history. We present model simulations of the Permian/Triassic climate transition that reproduce the ocean warming and oxygen (O2) loss indicated by the geologic record. The effect of these changes on animal survival is evaluated using the Metabolic Index (Φ), a measure of scope for aerobic activity governed by organismal traits sampled in diverse modern species. Modeled loss of aerobic habitat predicts lower extinction intensity in the tropics, a pattern confirmed with a spatially explicit analysis of the marine fossil record. The combined physiological stresses of ocean warming and O2 loss can account for more than half the magnitude of the “Great Dying.”

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HIV-1-infected persons with HLA-B27 and -B57 alleles commonly remain healthy for decades without antiretroviral therapy. Properties of CD8+ T cells restricted by these alleles considered to confer disease protection in these individuals are elusive but important to understand and potentially elicit by vaccination. To address this, we compared CD8+ T cell function induced by HIV-1 immunogens and natural infection using polychromatic flow cytometry. HIV-1-specific CD8+ T cells from all four uninfected immunized and 21 infected subjects secreted IFN-γ and TNF-α. However, CD8+ T cells induced by vaccination and primary infection, but not chronic infection, proliferated to their cognate epitopes. Notably, B27- and B57-restricted CD8+ T cells from nonprogressors exhibited greater expansion than those restricted by other alleles. Hence, CD8+ T cells restricted by certain protective alleles can resist replicative defects, which permits expansion and antiviral effector activities. Our findings suggest that the capacity to maintain CD8+ T cell proliferation, regardless of MHC-restriction, may serve as an important correlate of disease protection in the event of infection following vaccination.

Climate warming is expected to intensify hypoxia in the California Current System (CCS), threatening its diverse and productive marine ecosystem. We analyzed past regional variability and future changes in the Metabolic Index (Φ), a species-specific measure of the environment’s capacity to meet temperature-dependent organismal oxygen demand. Across the traits of diverse animals, Φ exhibits strong seasonal to interdecadal variations throughout the CCS, implying that resident species already experience large fluctuations in available aerobic habitat. For a key CCS species, northern anchovy, the long-term biogeographic distribution and decadal fluctuations in abundance are both highly coherent with aerobic habitat volume. Ocean warming and oxygen loss by 2100 are projected to decrease Φ below critical levels in 30 to 50% of anchovies’ present range, including complete loss of aerobic habitat—and thus likely extirpation—from the southern CCS. Aerobic habitat loss will vary widely across the traits of CCS taxa, disrupting ecological interactions throughout the region.

The dynamics of nitrogen (N) loss in the ocean’s oxygen-deficient zones (ODZs) are thought to be driven by climate impacts on ocean circulation and biological productivity. Here we analyze a data-constrained model of the microbial ecosystem in an ODZ and find that species interactions drive fluctuations in local- and regional-scale rates of N loss, even in the absence of climate variability. By consuming O2 to nanomolar levels, aerobic nitrifying microbes cede their competitive advantage for scarce forms of N to anaerobic denitrifying bacteria. Because anaerobes cannot sustain their own low-O2 niche, the physical O2 supply restores competitive advantage to aerobic populations, resetting the cycle. The resulting ecosystem oscillations induce a unique geochemical signature within the ODZ—short-lived spikes of ammonium that are found in measured profiles. The microbial ecosystem dynamics also give rise to variable ratios of anammox to heterotrophic denitrification, providing a mechanism for the unexplained variability of these pathways observed in the ocean.

Oxygen deficient zones (ODZs) below the ocean surface regulate marine productivity by removing bioavailable nitrogen (N). A complex microbial community mediates N loss, but the interplay of its diverse metabolisms is poorly understood. We present an ecosystem model of the North Pacific ODZ that reproduces observed chemical distributions yet predicts different ODZ structure, rates, and climatic sensitivity compared to traditional geochemical models. An emergent lower O2 limit for aerobic nitrification lies below the upper O2 threshold for anaerobic denitrification, creating a zone of microbial coexistence that causes a larger ODZ but slower total rates of N loss. The O2‐dependent competition for the intermediate nitrite produces gradients in its oxidation versus reduction, anammox versus heterotrophic denitrification, and the net ecological stoichiometry of N loss. The latter effect implies that an externally driven ODZ expansion should favor communities that more efficiently remove N, increasing the sensitivity of the N cycle to climate change.

Rising temperatures are associated with reduced body size in many marine species, but the biological cause and generality of the phenomenon is debated. We derive a predictive model for body size responses to temperature and oxygen (O 2 ) changes based on thermal and geometric constraints on organismal O 2 supply and demand across the size spectrum. The model reproduces three key aspects of the observed patterns of intergenerational size reductions measured in laboratory warming experiments of diverse aquatic ectotherms (i.e., the “temperature-size rule” [TSR]). First, the interspecific mean and variability of the TSR is predicted from species’ temperature sensitivities of hypoxia tolerance, whose nonlinearity with temperature also explains the second TSR pattern—its amplification as temperatures rise. Third, as body size increases across the tree of life, the impact of growth on O 2 demand declines while its benefit to O 2 supply rises, decreasing the size dependence of hypoxia tolerance and requiring larger animals to contract by a larger fraction to compensate for a thermally driven rise in metabolism. Together our results support O 2 limitation as the mechanism underlying the TSR, and they provide a physiological basis for projecting ectotherm body size responses to climate change from microbes to macrofauna. For small species unable to rapidly migrate or evolve greater hypoxia tolerance, ocean warming and O 2 loss in this century are projected to induce >20% reductions in body mass. Size reductions at higher trophic levels could be even stronger and more variable, compounding the direct impact of human harvesting on size-structured ocean food webs.

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