锡克
苦参素
生物
细胞生物学
信号转导
磷酸化
组蛋白H3
生物化学
组蛋白
酪氨酸激酶
白藜芦醇
基因
作者
Aidong Chen,Xinyong Zhang,Dongdong Hu,Sun XiaoYan,Yichun Gu,Yong Zhou,Chuanxin Su,Shi Liu,Caiyan Zhang,Guoping Lu,Qiwen Wu,Aidong Chen
出处
期刊:Research Square - Research Square
日期:2023-11-03
标识
DOI:10.21203/rs.3.rs-3426869/v1
摘要
Abstract During fungal infection, immune cells adapt their metabolic programs to support specialized anti-fungal effector functions. Nevertheless, the role of this process’s biochemical underpinnings is poorly understood. This study reports that fungal infection drives a switch from glycolysis to the serine synthesis pathway (SSP) and one-carbon metabolism by inducing the interaction of spleen tyrosine kinase (SYK) and phosphoglycerate dehydrogenase (PHGDH). As a result, PHGDH promotes SYK phosphorylation, leading to the recruitment of SYK to C-type lectin receptors (CLRs). The CLR/SYK complex initiates signaling cascades that lead to transcription factor activation and pro-inflammatory cytokine production. SYK activates SSP and one-carbon metabolism by inducing PHGDH activity. Then, one-carbon metabolism supports S-adenosylmethionine and histone H3 lysine 36 trimethylation to drive the production of pro-inflammatory cytokines and chemokines. These findings reveal the crosstalk between amino acid metabolism, epigenetic modification, and CLR signaling during fungal infection.
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