Soils contain the largest pool of terrestrial organic carbon (C) and are a major source of atmospheric carbon dioxide (CO2). Thus, they may play a key role in modulating climate change. Rising ...atmospheric CO2 is expected to stimulate plant growth and soil C input but may also alter microbial decomposition. The combined effect of these responses on long-term C storage is unclear. Combining meta-analysis with data assimilation, we show that atmospheric CO2 enrichment stimulates both the input (+19.8%) and the turnover of C in soil (+16.5%). The increase in soil C turnover with rising CO2 leads to lower equilibrium soil C stocks than expected from the rise in soil C input alone, indicating that it is a general mechanism limiting C accumulation in soil.
Serine-threonine kinase receptor-associated protein (STRAP) is a TGF-β receptor-interacting protein that participates in the regulation of cell proliferation and cell death in response to various ...stresses. Here, we demonstrate that STRAP phosphorylation plays an important role in determining the pro- or anti-apoptotic function of STRAP. Murine protein serine/threonine kinase 38 (MPK38) phosphorylates STRAP at Ser
188
via direct interaction. Complex formation between STRAP and MPK38 is mediated by Cys
152
and Cys
270
of STRAP and Cys
339
and Cys
377
of MPK38, suggesting the redox dependency of this interaction. MPK38-mediated STRAP Ser
188
phosphorylation contributes to the pro-apoptotic function of STRAP by modulating key steps in STRAP-dependent ASK1, TGF-β, p53, and PI3K/PDK1 signaling pathways. Moreover, knockdown of endogenous MPK38 using an inducible MPK38 shRNA system and in vivo activation of MPK38 by treatment of HEK293 and STRAP-null MEF cells with 1-chloro-2,4-dinitrobenzene (DNCB), a specific inhibitor of Trx reductase, provide evidence that STRAP Ser
188
phosphorylation plays a key role in STRAP-dependent cell death. Adenoviral delivery of MPK38 in mice also demonstrates that STRAP Ser
188
phosphorylation in the liver is tightly associated with cell death and proliferation through ASK1, TGF-β, p53, and PI3K/PDK1 pathways, resulting in apoptotic cell death.
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