BCL2L13 is a mammalian homolog of the yeast mitophagy receptor Atg32

Otsu, Kinya; Murakawa, Tomokazu; Yamaguchi, Osamu

doi:10.1080/15548627.2015.1084459

Cited by 73 publications

(41 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…By using an elegant experimental approach, Westerman and co-workers [69] revealed that Mmm1 and Atg8 interact and tether the mitochondrion destined for degradation to the ER and the isolation membrane of the growing phagophore (Figure 3). Consistent with this result, ERMES mutants have severe mitophagy defects [61] including accumulating immature autophagosomes. These results led the authors to hypothesize that these connections might provide an efficient supply of lipids from the ER to promote phagophore growth.…”

Section: Introductionsupporting

confidence: 55%

ER fatalities—The role of ER-mitochondrial contact sites in yeast life and death decisions

Smethurst

Cooper

2017

Mechanisms of Ageing and Development

View full text Add to dashboard Cite

Following extracellular stress signals, all eukaryotic cells choose whether to elicit a pro-survival or pro-death response. The decision over which path to take is governed by the severity and duration of the damage. In response to mild stress, pro-survival programs are initiated (unfolded protein response, autophagy, mitophagy) whereas severe or chronic stress forces the cell to abandon these adaptive programs and shift towards regulated cell death to remove irreversibly damaged cells. Both pro-survival and pro-death programs involve regulated communication between the endoplasmic reticulum (ER) and mitochondria. In yeast, recent data suggest this inter-organelle contact is facilitated by the endoplasmic reticulum mitochondria encounter structure (ERMES). These membrane contacts are not only important for the exchange of cellular signals, but also play a role in mitochondrial tethering during mitophagy, mitochondrial fission and mitochondrial inheritance. This review focuses on recent findings in yeast that shed light on how ER-mitochondrial communication mediates critical cell fate decisions.

show abstract

Section: Introductionsupporting

confidence: 55%

ER fatalities—The role of ER-mitochondrial contact sites in yeast life and death decisions

Smethurst

Cooper

2017

Mechanisms of Ageing and Development

View full text Add to dashboard Cite

show abstract

“…BCL2L13 has been identified as one of the functional counterparts of Atg32, since exogenous BCL2L13 expression can partially rescue a mitophagy defect in the atg32Δ yeast. Similar to the case of Atg32, the phosphorylation of Ser272 on BCL2L13 can also stimulate the binding of BCL2L13 to LC3 …”

Section: Mitophagy In Mammalsmentioning

confidence: 84%

Mechanisms and roles of mitophagy in neurodegenerative diseases

2019

View full text Add to dashboard Cite

Mitochondria are double‐membrane‐encircled organelles existing in most eukaryotic cells and playing important roles in energy production, metabolism, Ca 2+ buffering, and cell signaling. Mitophagy is the selective degradation of mitochondria by autophagy. Mitophagy can effectively remove damaged or stressed mitochondria, which is essential for cellular health. Thanks to the implementation of genetics, cell biology, and proteomics approaches, we are beginning to understand the mechanisms of mitophagy, including the roles of ubiquitin‐dependent and receptor‐dependent signals on damaged mitochondria in triggering mitophagy. Mitochondrial dysfunction and defective mitophagy have been broadly associated with neurodegenerative diseases. This review is aimed at summarizing the mechanisms of mitophagy in higher organisms and the roles of mitophagy in the pathogenesis of neurodegenerative diseases. Although many studies have been devoted to elucidating the mitophagy process, a deeper understanding of the mechanisms leading to mitophagy defects in neurodegenerative diseases is required for the development of new therapeutic interventions, taking into account the multifactorial nature of diseases and the phenotypic heterogeneity of patients.

show abstract

“…Mitophagy achieves its selectivity and specificity through a well established pathway composed of a serine/threonine kinase PINK1(phosphatase and tensin homolog–induced putative kinase 1) and an E3 ubiquitin ligase Parkin. The specificity is also mediated by a number of adaptors or receptors that are found in cytosol or on mitochondrial membranes, including sequestosome 1 (p62), histone deacetylase 6 (HDAC6), BCL2/adenovirus E1B interacting protein 3 (BNIP3), BNIP3-like (BNIP3L or NIX) [14, 15], FUN14 domain containing 1 (FUNDC1) [16], Bcl-2-like protein 13 (Bcl2L13) [17, 18], and Optineurin and Nuclear dot protein 52 (NDP52)[19]. Normally tightly coupled to mitophagy, the mitochondrial biogenesis is a process that generates new mitochondria to replenish the mitochondrial pool.…”

Section: Overviewmentioning

confidence: 99%

“…BCL2L13 is localized to outer mitochondrial membrane and interacts with LC3 through its WXXI motif, the LC3-interacting region required for mitophagy [17, 18]. Bcl2L13 induces mitophagy in a Parkin-independent manner without mitochondrial ubiquitination.…”

Section: Autophagy Mitophagy and Their Regulatory Pathwaysmentioning

confidence: 99%

Mitochondrial quality control in the diabetic heart

Liang

Kobayashi

2016

Journal of Molecular and Cellular Cardiology

View full text Add to dashboard Cite

Diabetes is a well known risk factor for heart failure. Diabetic heart damage is closely related to mitochondrial dysfunction and increased ROS generation. However, clinical trials have shown no effects of antioxidant therapies on heart failure in diabetic patients, suggesting that simply antagonizing existing ROS by antioxidants is not sufficient to reduce diabetic cardiac injury. A potentially more effective treatment strategy may be to enhance the overall capacity of mitochondrial quality control to maintain a pool of healthy mitochondria that are needed for supporting cardiac contractile function in diabetic patients. Mitochondrial quality is controlled by a number of coordinated mechanisms including mitochondrial fission and fusion, mitophagy and biogenesis. The mitochondrial damage consistently observed in the diabetic hearts indicates a failure of the mitochondrial quality control mechanisms. Recent studies have demonstrated a crucial role for each of these mechanisms in cardiac homeostasis and have begun to interrogate the relative contribution of insufficient mitochondrial quality control to diabetic cardiac injury. In this review, we will present currently available literature that links diabetic heart disease to the dysregulation of major mitochondrial quality control mechanisms. We will discuss the functional roles of these mechanisms in the pathogenesis of diabetic heart disease and their potentials for targeted therapeutical manipulation.

show abstract

BCL2L13 is a mammalian homolog of the yeast mitophagy receptor Atg32

Cited by 73 publications

References 1 publication

ER fatalities—The role of ER-mitochondrial contact sites in yeast life and death decisions

ER fatalities—The role of ER-mitochondrial contact sites in yeast life and death decisions

Mechanisms and roles of mitophagy in neurodegenerative diseases

Mitochondrial quality control in the diabetic heart

Contact Info

Product

Resources

About