Reply to Filadi et al.: Does Mitofusin 2 tether or separate endoplasmic reticulum and mitochondria?

We thank Filadi et al. for their comments (1) on our paper (2), where we address whether the discrepancies between their paper (3) and our original discovery of Mitofusin (Mfn) 2 as an endoplasmic reticulum (ER)–mitochondria tether (4) resulted from: ( i ) clonal effects of chronic Mfn2 ablation, ( ii ) proximity measurement inappropriateness, or ( iii ) changes in mitochondrial Ca2+ uniporter (MCU) levels in WT and Mfn2 −/−cells. Filadi et al. (1) conclude that we fell short in solving the issue and that our data reinforce Mfn2 function as an ER–mitochondria spacer (3). First, Filadi et al. (1) reason that we did not measure contacts number upon Mfn2 ablation. However, contact surface (which depends on contact number and extent) can be extracted from the ER–mitochondria contact coefficient and data in our paper (2). The average mitochondrial surface contacting ER … [↵][1]1To whom correspondence should be addressed. Email: luca.scorrano{at}unipd.it. [1]: #xref-corresp-1-1