Num1 is part of a protein complex that brings the mitochondrial, endoplasmic reticulum and plasma membranes together to form a membrane contact site (MCS) that tethers the mitochondria. Num1 also anchors the motor protein dynein at the cell cortex, and Laura Lackner's lab has previously shown that these two Num1 functions are linked. Here (White, Harper, Rosario et al., 2022), they find that Saccharomyces cerevisiae cells lacking Num1 form smaller colonies in respiratory growth conditions than their wild-type peers due to impaired mitochondrial function. They show that the deletion of domains required for the association of Num1 with either the mitochondrial (Num1ΔCC) or plasma (Num1ΔPH) membrane produces a phenotype similar to that observed in the Δnum1 cells. By attaching an anti-GFP nanobody to eisosome components, they cluster Num1ΔPH–GFP at the plasma membrane and show that this restoration of proper mitochondrial tethering is sufficient to rescue the Δnum1 respiratory growth defect. By contrast, restoring tethering in the absence of Num1 does not fully rescue the Δ num1 phenotype. They suggest this is because the dynein-anchoring role of Num1 also contributes to mitochondrial function, and ultimately go on to demonstrate that deletion of DYN1 attenuates the Δnum1 phenotype. This work reveals that Num1 affects mitochondrial function not only through mitochondrial tethering, but also through its role in dynein regulation.