Dysfunction of the motor subunit of the TIM23 translocase, the PAM complex located on the matrix side of the mitochondrial inner membrane in Saccharomyces cerevisiae, was shown to cause a decrease in mitochondrial protein import and precursor accumulation in the cytosol. We used an analogous model to study the non-mitochondrial response to defective mitochondrial import machinery in Caenorhabditis elegans in which we depleted DNJ-21 as the functional homolog of yeast Pam18. To gain a broader insight in potential changes in Caenorhabditis elegans proteome upon DNJ-21 depletion we performed a quantitative, label-free proteomics analysis. We compared protein levels upon knockdown of dnj-21 (dnj-21 RNAi) with control conditions (Empty vector RNAi). Synchronized N2 wild type worms were grown on NGM plates seeded with E. coli HT115(DE3) transformed with a construct targeting dnj-21 gene or with empty vector L4440 as a control.