2019
DOI: 10.7554/elife.44219
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Expression of WIPI2B counteracts age-related decline in autophagosome biogenesis in neurons

Abstract: Autophagy defects are implicated in multiple late-onset neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s, Huntington’s, and Parkinson’s diseases. Since aging is the most common shared risk factor in neurodegeneration, we assessed rates of autophagy in mammalian neurons during aging. We identified a significant decrease in the rate of constitutive autophagosome biogenesis during aging and observed pronounced morphological defects in autophagosomes in neurons from aged mic… Show more

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Cited by 63 publications
(46 citation statements)
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References 106 publications
(169 reference statements)
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“…The ATG12-ATG5-ATG16L1 complex is required for LC3 lipidation (Mizushima et al, 2001(Mizushima et al, , 2003Fujita et al, 2008). Though WIPI2 is a direct binding partner of ATG16L1 (Dooley et al, 2014), and in some cases WIPI2 potentiates LC3 lipidation (Polson et al, 2010;Dooley et al, 2014;Lystad et al, 2019;Stavoe et al, 2019), it is not required for LC3 lipidation induced by either starvation or monensin in HEK-293 cells (Lystad et al, 2019). ATG16L1 was previously shown to possess its own membrane-binding activity (Fletcher et al, 2018;Lystad et al, 2019).…”
Section: Discussionmentioning
confidence: 99%
“…The ATG12-ATG5-ATG16L1 complex is required for LC3 lipidation (Mizushima et al, 2001(Mizushima et al, , 2003Fujita et al, 2008). Though WIPI2 is a direct binding partner of ATG16L1 (Dooley et al, 2014), and in some cases WIPI2 potentiates LC3 lipidation (Polson et al, 2010;Dooley et al, 2014;Lystad et al, 2019;Stavoe et al, 2019), it is not required for LC3 lipidation induced by either starvation or monensin in HEK-293 cells (Lystad et al, 2019). ATG16L1 was previously shown to possess its own membrane-binding activity (Fletcher et al, 2018;Lystad et al, 2019).…”
Section: Discussionmentioning
confidence: 99%
“…Wipi2, which is involved in autophagy in DRG neurons (Stavoe et al, 2019), a process 281 argued to reduce the pain associated with sciatic nerve injury (Chen et al, 2018). PEP1 282 neurons selectively induce Ano1, which promotes pain hypersensitivity (Lee et al, 2014).…”
Section: Classification Of Neuronal Subtypes After Axotomy 199mentioning
confidence: 99%
“…Recently, patients with mutations in the WIPI2 gene have been described with multisystemic clinical features, primarily, neurological and skeletal deficiencies that are characterized by severe mental retardation and short stature (Jelani et al, 2019). Notably, WIPI2 overexpression prevents age-related autophagy decline in dorsal root ganglion neurons (Stavoe et al, 2019). Patients with mutations in the genes WIPI3 (WDR45B) or WIPI4 (WDR45) show severe and progressive neurodegenerative phenotypes (Haack et al, 2012;Hayflick et al, 2013;Saitsu et al, 2013;Suleiman et al, 2018).…”
Section: Defects In the Autophagic Machinerymentioning
confidence: 99%