The ribosome not only functions as a protein manufacturing machine but also plays a regulatory role in protein synthesis. The gene RPS10 encodes the small ribosomal subunit protein S10, a crucial component of the 40S ribosomal subunit. Malgorzata Kwasniak-Owczarek et al. demonstrated that defects in mitochondrial ribosomal protein S10, induced by RNAi, have significant effects on mitochondrial function based on ribo-seq and RNA-seq data. Defects in mitochondrial ribosomal protein S10 led to a marked downregulation of mitochondrial oxidative phosphorylation and reduced translation efficiency of proteins associated with respiration. Furthermore, the study found that defects in mitochondrial ribosomal protein S10 also affect the translation of mitochondrial transcripts. 

In this project, our goal is to replicate the modified mitochondrial gene expression profile using the sequencing data from the previously mentioned study. Additionally, we aim to perform enrichment analysis to investigate potential pathways and metabolic events influenced by the dysregulation of RPS10. This exploration will shed light on the potential roles of RPS10 in mitochondrial energy generation. Understanding the involvement of RPS10 in human mitochondrial functions is crucial for addressing certain inherited diseases, such as Diamond-Blackfan anemia, which stem from mitochondrial dysfunction. Thus, our efforts will focus on identifying human homologs of differentially expressed genes in Arabidopsis due to RPS10 alteration. Subsequently, we will delve into potential signaling pathways that may be impacted by RPS10 dysregulation.