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Macroautophagy, commonly referred to as autophagy, is an evolutionarily conserved cellular process that plays a crucial role in maintaining cellular homeostasis. It orchestrates the delivery of dysfunctional or surplus cellular materials to the vacuole or lysosome for degradation and recycling, particularly during adverse conditions. Over the past few decades, research has unveiled intricate regulatory mechanisms governing autophagy through various post-translational modifications (PTMs). Among these PTMs, acetylation modification has emerged as a focal point in yeast and animal studies. It plays a pivotal role in autophagy by directly targeting core components within the central machinery of autophagy, including autophagy initiation, nucleation, phagophore expansion, and autophagosome maturation. Additionally, acetylation modulates autophagy at the transcriptional level by modifying histones and transcription factors. Despite its well-established significance in yeast and mammals, the role of acetylation in plant autophagy remains largely unexplored, and the precise regulatory mechanisms remain enigmatic. In this comprehensive review, we summarize the current understanding of the function and underlying mechanisms of acetylation in regulating autophagy across yeast, mammals, and plants. We particularly highlight recent advances in deciphering the impact of acetylation on plant autophagy. These insights not only provide valuable guidance but also inspire further scientific inquiries into the intricate role of acetylation in plant autophagy.
Macroautophagy, commonly referred to as autophagy, is an evolutionarily conserved cellular process that plays a crucial role in maintaining cellular homeostasis. It orchestrates the delivery of dysfunctional or surplus cellular materials to the vacuole or lysosome for degradation and recycling, particularly during adverse conditions. Over the past few decades, research has unveiled intricate regulatory mechanisms governing autophagy through various post-translational modifications (PTMs). Among these PTMs, acetylation modification has emerged as a focal point in yeast and animal studies. It plays a pivotal role in autophagy by directly targeting core components within the central machinery of autophagy, including autophagy initiation, nucleation, phagophore expansion, and autophagosome maturation. Additionally, acetylation modulates autophagy at the transcriptional level by modifying histones and transcription factors. Despite its well-established significance in yeast and mammals, the role of acetylation in plant autophagy remains largely unexplored, and the precise regulatory mechanisms remain enigmatic. In this comprehensive review, we summarize the current understanding of the function and underlying mechanisms of acetylation in regulating autophagy across yeast, mammals, and plants. We particularly highlight recent advances in deciphering the impact of acetylation on plant autophagy. These insights not only provide valuable guidance but also inspire further scientific inquiries into the intricate role of acetylation in plant autophagy.
(1) Background: Bovine viral diarrhea virus (BVDV) causes calf diarrhea, bovine respiratory syndrome, and cow abortion, resulting in substantial economic losses in the cattle industry. Owing to its persistent infection mechanism, BVDV is a major challenge in the treatment of cattle. (2) Methods: To determine how metformin (Met) inhibits the interaction between BVDV and host cells, we treated BVDV-infected cells with Met. We then performed an RNA sequencing (RNA-seq) analysis of Met-treated cells infected with BVDV to identify differentially expressed genes (DEGs). Consequently, the RNA-seq results were validated through real-time quantitative PCR (qPCR). (3) Results: Our analysis revealed 3169 DEGs in the Met-treated cells (Met group) vs. the negative controls (NC group) and 2510 DEGs in the BVDV-infected cells after pretreatment with Met (MetBVDV group) vs. the BVDV-infected cells (BVDV group). The DEGs were involved in MDBK interactions during BVDV infection, as indicated by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The potential interactions of the DEGs were confirmed via a protein–protein interaction (PPI) network. Met treatment induced autophagy signaling activity and the expression of the autophagy-related genes ATG2A, ATG4B, ATG10, and ATG12 in BVDV-infected Met-pretreated cells. (4) Conclusions: We found that the host transcriptomic profile was affected by BVDV infection and Met pretreatment. These findings offer valuable new insights and provide support for future studies on the inhibition of BVDV replication by Met.
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