Table 1. Regulation of Mitochondrial Dynamics.

	Control Mechanism	Outcome	Reference
Fission
	Global Cellular Control
	Ubiquitination of DRP1 (MARCH V)	Inhibition of Fission	[84]
	cAMP Dependent Phosphorylation of DRP1	Inhibition of Fission	[85]
	Calcium dependent recruitment of DRP1 from Cytosol	Fission induced by global calcium	[34] [84]; [36]
	Dephosphorylation of DRP1 by Calcineurin regulates translocation to mitochondria	Fission induced elevated cytosolic calcium	[85] [86]
	Increase of Bax/Bak induces Fission. Bax and Bak in healthy cell controls fusion through Mfn2	Interacts at mitochondrial fission sites to promote fission	[37;38]
	Sumoylation of DRP1 at fission sites	Sumoylation protects DRP1 from degradation and allows fission to proceed	[40] [41]
	Local Organelle Control
	Loss of Membrane potential leads to OPA1 processing by metalloproteases	Increased OPA1 processing inhibits fusion of individual mitochondrion	[46] [50] [51] [45]
	Increased OPA1 processing in response to local membrane potential and ATP levels	OPA1 processing inhibits fusion and induces mitophagy	[6;44;50]
Fusion
	Global Cellular Control
	Activation of PGC1a/PGC-1b/ERRa induces MFN2 mRNA. PGC-1b induces mitochondrial fusion through Mfn2.	Increased Fusion/Mitochondrial Biogenesis	[87] [10]
	BID disrupts the OPA1 cristae junction complex	The size of cristae junction is regulated independently of OPA1 mitochondrial fusion activity	[88]
	Mito tubularization and network fusion at G1-S of cell cycle.	G1-S stimulates global mitochondrial fusion, mitosis stimulates fission	[16;20] [19]
	Local Organelle Control
	Functional interaction of OPA1 with MFN1.	Functional interaction of Mfn1 and Opa1 but not Mfn2.	[43;89]
	OPA1 processing by Metalloproteases blocks fusion	Fusion inhibited at the local level by protease activity	[50], [51], [45] [89] [44]
	Low Local GTP level induces outer membrane tethering	Initial fusion promoted in energy deficient environments	[71]
	High Intra-mitochondrial GTP levels required for inner membrane fusion	Complete fusion regulated by energetic status	[71]
	Mitochondrial movement on microtubules is essential for fusion	Inhibition of movement arrests fusion	[24]
Solitary Period
	Global Cellular Control
	Increase of cellular calcium increases mitochondrial motility and fusion (Miro)	Release of cellular calcium stores increases mitochondrial movement	[75] [90]
	Global ADP levels increase Mitochondrial movement to synapses	ADP signals mitochondrial motility	[81]
	GPCR Ga12 is expressed in mitochondria and regulates motility	GPCR sensitive to GDP/GTP levels regulate mitochondrial motility	[82]
	Local Organelle Control
	Local ATP level/membrane potential regulates motility	Increased energetic capacity increases movement	[75]
	Mito movement along Microtubules occurs in an energy dependent manner	Individual mitochondria move at different rates along microtubules based on ATP levels	[78] [79]; [75]
	Local redox status of Mitochondria impacts MMP and Velocity of movement	Elevated Oxidation leads to Loss of MMP. Loss of MMP leads to increased motility	Gerenscer and Nicholls 22