Table 1.

Overview of effects of mTORC1 and downstream effectors on mitochondrial biogenesis. For each study, the cell/tissue type, the target and the method used to interfere with the target are summarized as well as the effects observed. MEFs, mouse embryonic fibroblasts.

cells	target	method	effect	references
(a) in vitro studies
MEFs	TSC2	knockout	enhanced interaction YY1 and PGC-1α	[54]
			increased oxygen consumption
			increased mitochondrial DNA content
muscle cells	mTORC1	rapamycin	decreased PGC-1α-mediated gene transcription	[54]
			decreased oxygen consumption
			decreased mitochondrial DNA content
	YY1	knockdown	decreased mitochondrial gene expression
			decreased oxygen consumption
			decreased mitochondrial DNA content
Jurkat/HEK293	mTORC1	rapamycin	decreased oxygen consumption	[44]
			decreased mitochondrial membrane potential
	Raptor	knockdown	decreased oxygen consumption
			decreased mitochondrial membrane potential
	YY1	overexpression	increased mitochondrial gene expression	[54]
tissue	target	method	effect	references
(b) in vivo studies
muscle	YY1	deletion	decreased OXPHOS	[55]
			decreased mitochondrial protein content
			exercise intolerance
	PGC-1α	overexpression	increased OXPHOS	[56]
			improved insulin sensitivity
	mTOR	deletion	decreased oxidative capacity	[57]
			altered mitochondrial morphology
			muscular dystrophy
	Raptor	deletion	decreased oxidative capacity	[58]
			altered mitochondrial morphology
			muscular dystrophy
	S6K1	deletion	AMPK activation	[59]
			increased AMP/ATP ratio
			energy stress
	AMPK	deletion	decreased expression PGC-1α	[60]
			decreased mitochondrial biogenesis
adipocytes	Raptor	deletion	reduction size and number adipocytes	[61]
			lean mice
whole body	S6K1	deletion	increased mitochondrial content skeletal muscle	[62]
			increased mitochondrial content adipocytes
			reduction size and number adipocytes
			lean mice