2019
DOI: 10.1038/s41586-019-1738-6
|View full text |Cite
|
Sign up to set email alerts
|

Lipid signalling drives proteolytic rewiring of mitochondria by YME1L

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

12
117
0
1

Year Published

2019
2019
2024
2024

Publication Types

Select...
8
2

Relationship

0
10

Authors

Journals

citations
Cited by 122 publications
(130 citation statements)
references
References 51 publications
12
117
0
1
Order By: Relevance
“…It is also suggested that PE homeostasis is relevant for fusion, as both S-Mgm1 protein and mitochondrial fusion are decreased when mitochondrial PE levels are low (Chan and McQuibban, 2012;Joshi et al, 2012). Recently, a lipid signaling cascade dependent on the PA phosphatase LIPIN1 was found to modulate mitochondrial PE abundance (MacVicar et al, 2019). mTORC1 inhibition by hypoxia or amino acid starvation leads to LIPIN1 activation, decreasing PA amounts and ultimately mitochondrial PE levels, which then promotes proteolysis by YME1L (MacVicar et al, 2019;Peterson et al, 2011).…”
Section: Mitochondrial Fusionmentioning
confidence: 99%
“…It is also suggested that PE homeostasis is relevant for fusion, as both S-Mgm1 protein and mitochondrial fusion are decreased when mitochondrial PE levels are low (Chan and McQuibban, 2012;Joshi et al, 2012). Recently, a lipid signaling cascade dependent on the PA phosphatase LIPIN1 was found to modulate mitochondrial PE abundance (MacVicar et al, 2019). mTORC1 inhibition by hypoxia or amino acid starvation leads to LIPIN1 activation, decreasing PA amounts and ultimately mitochondrial PE levels, which then promotes proteolysis by YME1L (MacVicar et al, 2019;Peterson et al, 2011).…”
Section: Mitochondrial Fusionmentioning
confidence: 99%
“…1 ). However, stresses such as hypoxia or nutrient deprivation induce a lipid signaling cascade upon inactivation of mechanistic target of rapamycin complex 1 (mTORC1) to reduce PE levels at the IMM, leading to activation of YME1L-mediated proteolysis of mitochondrial proteins and subsequent inhibition of mitochondrial biogenesis ( MacVicar et al, 2019 ). This involves activation of LIPIN1, a substrate of mTORC1 that is phosphorylated and hence inhibited under basal conditions (e.g., available oxygen and nutrients).…”
Section: Mitochondrial Lipid Signalingmentioning
confidence: 99%
“…Regulation of mitochondrial dynamics due to processing of the dynamin-like GTPase OPA1 is perhaps one of the best characterised roles of YME1L (76,106). Changes to OPA1 processing has been implicated in altering mitochondrial morphology in response to different cellular stresses, metabolic and environmental demands (105,107,108). Whilst mitochondrial morphology has been reported to be modified during infection with Listeria monocytogenes, Vibrio cholerae and L. pneumophila, thus far, no study has demonstrated any mitochondrial network alterations during C. burnetii infection (35,(109)(110)(111).…”
Section: Discussionmentioning
confidence: 99%