Crosstalk between the Secretory and Autophagy Pathways Regulates Autophagosome Formation

Davis, Saralin; Wang, Juan; Ferro‐Novick, Susan

doi:10.1016/j.devcel.2017.03.015

Cited by 63 publications

(55 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…COPII is subject to control by phosphorylation during these events including modification of Sec23 (Gan et al 2017) and Sec24 (Davis et al 2016). This has been reviewed in more detail elsewhere (Davis et al 2017). A further possible point of integration between COPII and autophagy is Tectonin β-propeller containing protein 2 [TECPR2, (Stadel et al 2015)].…”

Section: Copii and Proteostasis: Autophagy And The Uprmentioning

confidence: 99%

COPII-dependent ER export in animal cells: adaptation and control for diverse cargo

McCaughey

Stephens

2018

Histochem Cell Biol

View full text Add to dashboard Cite

The export of newly synthesized proteins from the endoplasmic reticulum is fundamental to the ongoing maintenance of cell and tissue structure and function. After co-translational translocation into the ER, proteins destined for downstream intracellular compartments or secretion from the cell are sorted and packaged into transport vesicles by the COPII coat protein complex. The fundamental discovery and characterization of the pathway has now been augmented by a greater understanding of the role of COPII in diverse aspects of cell function. We now have a deep understanding of how COPII contributes to the trafficking of diverse cargoes including extracellular matrix molecules, developmental signalling proteins, and key metabolic factors such as lipoproteins. Structural and functional studies have shown that the COPII coat is both highly flexible and subject to multiple modes of regulation. This has led to new discoveries defining roles of COPII in development, autophagy, and tissue organization. Many of these newly emerging features of the canonical COPII pathway are placed in a context of procollagen secretion because of the fundamental interest in how a coat complex that typically generates 80-nm transport vesicles can package a cargo reported to be over 300 nm. Here we review the current understanding of COPII and assess the current consensus on its role in packaging diverse cargo proteins.

show abstract

Section: Copii and Proteostasis: Autophagy And The Uprmentioning

confidence: 99%

COPII-dependent ER export in animal cells: adaptation and control for diverse cargo

McCaughey

Stephens

2018

Histochem Cell Biol

View full text Add to dashboard Cite

show abstract

“…A conserved family of autophagy-related genes (ATGs) has been identified as the key machinery for autophagosome formation and maturation. 12 In mammalian cells, Unc-51 like autophagy activating kinase (ULK1) is critical for the initiation of autophagosome where it forms a complex with the proteins ATG13, ATG17, and ATG101. 13 This activated ULK1 complex then recruits the transmembrane protein ATG9 followed by the UV radiation resistance-associated gene protein (UVRAG) containing a phosphatidylinositol 3-kinase (PIK3) complex.…”

Section: A Brief Overview Of Autophagymentioning

confidence: 99%

“…This process itself has been studied and reviewed extensively elsewhere, but, in brief, it consists of three main stages: initiation (induction), maturation, and lysosomal fusion (completion). A conserved family of autophagy‐related genes (ATGs) has been identified as the key machinery for autophagosome formation and maturation . In mammalian cells, Unc‐51 like autophagy activating kinase (ULK1) is critical for the initiation of autophagosome where it forms a complex with the proteins ATG13, ATG17, and ATG101 .…”

Section: Introductionmentioning

confidence: 99%

Cellular and molecular mechanisms involved in the resolution of innate leukocyte inflammation

Rahtes

Geng

Lee

et al. 2018

Journal of Leukocyte Biology

View full text Add to dashboard Cite

Inflammation is a host response to infection or damage and is vital for clearing pathogens and host debris. When this resolution fails to occur, chronic inflammation ensues. Chronic inflammation is typically characterized as a low-grade, persistent inflammatory process that can last for months or even years. This differs from acute inflammation, which is typically a fast, robust response to a stimulus followed by resolution with return to homeostasis. Inflammation resolution occurs through a variety of cellular processes and signaling components that act as “brakes” to keep inflammation in check. In cases of chronic inflammation, these “brakes” are often dysfunctional. Due to its prevalent association with chronic diseases, there is growing interest in characterizing these negative regulators and their cellular effects in innate leukocytes. In this review, we aim to describe key cellular and molecular homeostatic regulators of innate leukocytes, with particular attention to the emerging regulatory processes of autophagy and lysosomal fusion during inflammation resolution.

show abstract

“…Originally, it was thought that the autophagosome only derives from mobile cytoplasmic vesicles characterized by the transmembrane protein ATG9, which are recruited to the ER. However, it has become clear that, in response to starvation, additional sources of membrane are necessary for the formation and growth of the autophagosome (Davis et al, 2017;Hurley and Young, 2017;Wang et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…COPII vesicles emerge from specialized domains of the ER called ER exit sites (ERES) (Zanetti et al, 2011). However, in response to starvation, when the secretory pathway is inhibited (Wang et al, 2014;Zacharogianni et al, 2014;Zacharogianni et al, 2011) and there is an urgent need for membranes to form autophagosomes, ERES enlarge and patches along the ERGIC to function in autophagosome biogenesis (Davis et al, 2017;Egan et al, 2015;Ge et al, 2017;Ge et al, 2014;Hurley and Young, 2017;Sanchez-Wandelmer et al, 2015). In mammals, disruption of ERES inhibits autophagosome biogenesis at an early stage (Stadel et al, 2015;Zoppino et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

The ULK1-FBXW5-SEC23B nexus controls autophagy

Pagano

Jeong

Simoneschi

et al. 2018

Preprint

View full text Add to dashboard Cite

In response to nutrient deprivation, the cell needs to mobilize an extensive amount of membrane to form and grow the autophagosome, allowing the progression of autophagy.By providing membranes and a source for LC3 lipidation, COPII (Coat Protein Complex II) localizes to the endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) and promotes autophagosome biogenesis. However, the molecular mechanisms that, in response to starvation, divert COPII from the secretory pathway to the autophagic pathway are largely unknown. Here, we show that the F-box protein FBXW5 targets SEC23B, a component of COPII, for proteasomal degradation and that this event limits the autophagic flux in the presence of nutrients. In response to starvation, ULK1 phosphorylates SEC23B on Serine 186, preventing the interaction of SEC23B with FBXW5 and, therefore, inhibiting its degradation. Phosphorylated and stabilized SEC23B associates with SEC24A and SEC24B, but not SEC24C and SEC24D, and they re-localize to the ERGIC, promoting autophagic flux. Induction of autophagy and localization of both SEC23B and SEC24B to the ERGIC in response to nutrient deprivation are significantly reduced in SEC23B(S186A) knock-in cells. We propose that, in the presence of nutrients, FBXW5 limits COPII-mediated autophagosome biogenesis. Inhibition of this event by ULK1 ensures efficient execution of the autophagic cascade in response to nutrient starvation.

show abstract

Crosstalk between the Secretory and Autophagy Pathways Regulates Autophagosome Formation

Cited by 63 publications

References 101 publications

COPII-dependent ER export in animal cells: adaptation and control for diverse cargo

COPII-dependent ER export in animal cells: adaptation and control for diverse cargo

Cellular and molecular mechanisms involved in the resolution of innate leukocyte inflammation

The ULK1-FBXW5-SEC23B nexus controls autophagy

Contact Info

Product

Resources

About