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Agriculture has become a main source of greenhouse gas emissions globally, so limiting agricultural carbon emissions is an important part of achieving carbon neutrality in China. The reduction of agricultural carbon emissions needs the support of green credit. This paper explores the spatial effect and mechanism of green credit on agricultural carbon emissions. Specifically, based on panel data of 30 Chinese provinces from 2009 to 2019, the relationship between green credit and agricultural carbon emissions is empirically analyzed using spatial econometric and mediating effect models. The results show that green credit has a significant inhibitory effect on agricultural carbon emissions. Meanwhile, green credit can also limit agricultural carbon emissions in surrounding areas through spatial spillover effects. Moreover, the study reveals that green credit can indirectly suppress agricultural carbon emissions by promoting agricultural green technology innovation. Based on the above conclusions, this paper puts forward policy recommendations for the development of green credit and the reduction of agricultural carbon emissions.

Quiescent satellite cells are myogenic progenitors that enable regeneration of skeletal muscle. One of the early events of satellite cell activation following myotrauma is the induction of the myogenic regulatory factor MyoD, which eventually induces terminal differentiation and muscle function gene expression. The purpose of this study was to elucidate the mechanism by which MyoD is induced during activation of satellite cells in mouse muscle undergoing regeneration. We show that Six1, a transcription factor essential for embryonic myogenesis, also regulates MyoD expression in muscle progenitor cells. Six1 knock-down by RNA interference leads to decreased expression of MyoD in myoblasts. Chromatin immunoprecipitation assays reveal that Six1 binds the Core Enhancer Region of MyoD. Further, transcriptional reporter assays demonstrate that Core Enhancer Region reporter gene activity in myoblasts and in regenerating muscle depends on the expression of Six1 and on Six1 binding sites. Finally, we provide evidence indicating that Six1 is required for the proper chromatin structure at the Core Enhancer Region, as well as for MyoD binding at its own enhancer. Together, our results reveal that MyoD expression in satellite cells depends on Six1, supporting the idea that Six1 plays an important role in adult myogenesis, in addition to its role in embryonic muscle formation.