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2017 ; 61
(6
): 565-584
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mTORC1 as the main gateway to autophagy
#MMPMID29233869
Rabanal-Ruiz Y
; Otten EG
; Korolchuk VI
Essays Biochem
2017[Dec]; 61
(6
): 565-584
PMID29233869
show ga
Cells and organisms must coordinate their metabolic activity with changes in
their environment to ensure their growth only when conditions are favourable. In
order to maintain cellular homoeostasis, a tight regulation between the synthesis
and degradation of cellular components is essential. At the epicentre of the
cellular nutrient sensing is the mechanistic target of rapamycin complex 1
(mTORC1) which connects environmental cues, including nutrient and growth factor
availability as well as stress, to metabolic processes in order to preserve
cellular homoeostasis. Under nutrient-rich conditions mTORC1 promotes cell growth
by stimulating biosynthetic pathways, including synthesis of proteins, lipids and
nucleotides, and by inhibiting cellular catabolism through repression of the
autophagic pathway. Its close signalling interplay with the energy sensor
AMP-activated protein kinase (AMPK) dictates whether the cell actively favours
anabolic or catabolic processes. Underlining the role of mTORC1 in the
coordination of cellular metabolism, its deregulation is linked to numerous human
diseases ranging from metabolic disorders to many cancers. Although mTORC1 can be
modulated by a number of different inputs, amino acids represent primordial cues
that cannot be compensated for by any other stimuli. The understanding of how
amino acids signal to mTORC1 has increased considerably in the last years;
however this area of research remains a hot topic in biomedical sciences. The
current ideas and models proposed to explain the interrelationship between amino
acid sensing, mTORC1 signalling and autophagy is the subject of the present
review.
|Amino Acids/metabolism
[MESH]
|Animals
[MESH]
|Autophagy/genetics/*physiology
[MESH]
|Humans
[MESH]
|Lysosomes/metabolism
[MESH]
|Mechanistic Target of Rapamycin Complex 1/genetics/*metabolism
[MESH]
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