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[1] The major increase in atmospheric methane (CH 4 ) concentration during the last glacial-interglacial transition provides a useful example for understanding the interactions and feedbacks among Earth's climate, biosphere carbon cycling, and atmospheric chemistry. However, the causes of CH 4 doubling during the last deglaciation are still uncertain and debated. Although the ice-core data consistently suggest a dominant contribution from northern high-latitude wetlands in the early Holocene, identifying the actual sources from the ground-based data has been elusive. Here we present data syntheses and a case study from Alaska to demonstrate the importance of northern wetlands in contributing to high atmospheric CH 4 concentration in the early Holocene. Our data indicate that new peatland formation as well as peat accumulation in northern high-latitude regions increased more than threefold in the early Holocene in response to climate warming and the availability of new habitat as a result of deglaciation. Furthermore, we show that marshes and wet fens that represent early stages of wetland succession were likely more widespread in the early Holocene. These wetlands are associated with high CH 4 emissions due to high primary productivity and the presence of emergent plant species that facilitate CH 4 transport to the atmosphere. We argue that early wetland succession and rapid peat accumulation and expansion (not simply initiation) contributed to high CH 4 emissions from northern regions, potentially contributing to the sharp rise in atmospheric CH 4 at the onset of the Holocene.

Innate immune cells play important roles in tissue injury and repair following acute myocardial infarction (MI). Although reprogramming of macrophage metabolism has been observed during inflammation and resolution phases, the mechanistic link to macrophage phenotype is not fully understood. In this study, we found myeloid specific deletion of mitochondrial Complex I protein Ndufs4 (mKO) reproduced the pro-inflammatory metabolic profile in macrophages and exaggerated the response to lipopolysacharride. Moreover, mKO mice showed increased mortality, poor scar formation and worsened cardiac function 30 days post-MI. We observed a greater inflammatory response in mKO on day 1 followed by increased cell death of infiltrating macrophages and blunted transition to reparative phase during day 3-7 post-MI. Efferocytosis is impaired in mKO macrophages leading to lower expression of anti-inflammatory cytokine and tissue repair factors, which suppressed the proliferation/activation of myofibroblasts in the infarct area. Mitochondria-targeted ROS scavenging rescued these impairments and improved myofibroblast function in vivo and reduced post-MI mortality in mKO mice. Together these results reveal a critical role of mitochondria in inflammation resolution and tissue repair via modulating efferocytosis and crosstalk with fibroblasts. The findings are significant for post-MI recovery as well as for other inflammatory conditions.