Mitochondrial positioning supports localized energy and signaling requirements. Miro1 is necessary for attachment of mitochondria to microtubule motor proteins for trafficking. When Miro1 is deleted (Miro1-/-) from mouse embryonic fibroblasts (MEFs), mitochondria become sequestered to the perinuclear space, disrupting subcellular signaling gradients. Here, we show that Miro1-/- MEFs grow slower compared to Miro1+/+ and Miro1-/- MEFs stably re-expressing a Myc-Miro1 plasmid. Miro1-/- MEFs have a decreased percentage of cells in G1 and increased cells in S phase. We conducted the first ever RNA sequencing experiment dependent upon Miro1 expression and found differentially expressed genes related to MAP Kinase signaling, cell proliferation and migration. ERK1/2 phosphorylation is elevated both spatially and temporally following serum stimulation in Miro1-/- MEFs, while the expression levels and oxidation of the Dual Specificity Phosphatases (DUSP1-6) is unchanged. Lastly, we found the oxidation status of ERK1/2 is increased in Miro1-/- MEFs compared to Miro1+/+ and Myc-Miro1 MEFs. These results highlight transcriptional control based off Miro1 expression and demonstrate the dynamic regulation of ERK1/2 upon deletion of Miro1 which may support the observed cell cycle and proliferation defects.