AMBRA1-regulated autophagy in vertebrate development

Antonioli, Manuela; Albiero, Federica; Fimia, Gian María; Piacentini, Mauro

doi:10.1387/ijdb.150057mp

Cited by 13 publications

(5 citation statements)

References 99 publications

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“…The study of genetically modified mice has shed light on the roles played by the genes involved in autophagy. Ambra1 is an essential gene for the development of the mouse central nervous system, the deficiency of which impairs autophagy and induces aberrant neuronal proliferation (Fimia et al, 2007; Antonioli et al, 2015). Different mutations in genes that participate in the autophagy machinery have shown that autophagy is needed for terminal neuronal differentiation, and specifically for axonal outgrowth and guidance.…”

Section: Developmental Autophagymentioning

confidence: 99%

Autophagy in the Vertebrate Inner Ear

Magariños

Pulido

Aburto

et al. 2017

Front. Cell Dev. Biol.

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Autophagy is a conserved catabolic process that results in the lysosomal degradation of cell components. During development, autophagy is associated with tissue and organ remodeling, and under physiological conditions it is tightly regulated as it plays a housekeeping role in removing misfolded proteins and damaged organelles. The vertebrate inner ear is a complex sensory organ responsible for the perception of sound and for balance. Cell survival, death and proliferation, as well as cell fate specification and differentiation, are processes that are strictly coordinated during the development of the inner ear in order to generate the more than a dozen specialized cell types that constitute this structure. Here, we review the existing evidence that implicates autophagy in the generation of the vertebrate inner ear. At early stages of chicken otic development, inhibiting autophagy impairs neurogenesis and causes aberrant otocyst morphogenesis. Autophagy provides energy for the clearing of dying cells and it favors neuronal differentiation. Moreover, autophagy is required for proper vestibular development in the mouse inner ear. The autophagy-related genes Becn1, Atg4g, Atg5, and Atg9, are expressed in the inner ear from late developmental stages to adulthood, and Atg4b mutants show impaired vestibular behavior associated to defects in otoconial biogenesis that are also common to Atg5 mutants. Autophagic flux appears to be age-regulated, augmenting from perinatal stages to young adulthood in mice. This up-regulation is concomitant with the functional maturation of the hearing receptor. Hence, autophagy can be considered an intracellular pathway fundamental for in vertebrate inner ear development and maturation.

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Section: Developmental Autophagymentioning

confidence: 99%

Autophagy in the Vertebrate Inner Ear

Magariños

Pulido

Aburto

et al. 2017

Front. Cell Dev. Biol.

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“…Aegypti . AMBRA1 is a novel regulator for phagophore nucleation, and the knockout of AMBRA1 in mice resulted in autophagy inhibition and embryonic lethality ( 5 – 7 ). ATG8 is essential for autophagic vesicle formation and has been utilized as a marker for autophagic activity in previous studies ( 9 ).…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence of a pivotal role of AMBRA1 protein in autophagy and apoptosis has been reported in vertebrate neurodevelopment in previous years ( 6 ). A mutation in the AMBRA1 gene impairs the regulation of autophagy in mice and alters the balance between apoptotic cell death and proliferation and resulting in embryonic lethality ( 7 ). From yeast to mammals, two conjugation systems are involved in the autophagosome formation process: the formation of the ATG12-5-16 complex on the isolation membrane and the localization of ATG8-PE to the isolation membrane.…”

Section: Introductionmentioning

confidence: 99%

Autophagy genes AMBRA1 and ATG8 play key roles in midgut remodeling of the yellow fever mosquito, Aedes aegypti

Albishi

Palli

2023

Front. Insect Sci.

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The function of two autophagy genes, an activating molecule BECN1 regulated autophagy (AMBRA1) and autophagy-related gene 8 (ATG8) in the midgut remodeling of Aedes aegypti was investigated. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis of RNA samples collected from the last instar larvae and pupae showed that these two genes are predominantly expressed during the last 12 h and first 24 h of the last larval and pupal stages, respectively. Stable ecdysteroid analog induced and juvenile hormone (JH) analog suppressed these genes. RNA interference (RNAi) studies showed that the ecdysone-induced transcription factor E93 is required for the expression of these genes. JH-induced transcription factor krüppel homolog 1 (Kr-h1) suppressed the expression of these genes. RNAi-mediated silencing of AMBRA1 and ATG8 blocked midgut remodeling. Histological studies of midguts from insects at 48 h after ecdysis to the final larval stage and 12 h after ecdysis to the pupal stage showed that ATG gene knockdown blocked midgut remodeling. AMBRA1 and ATG8 double-stranded (dsRNA)-treated insects retained larval midgut cells and died during the pupal stage. Together, these results demonstrate that ecdysteroid induction of ATG genes initiates autophagy programmed cell death during midgut remodeling. JH inhibits midgut remodeling during metamorphosis by interfering with the expression of ATG genes.

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“…Autophagy-related proteins 2 and 9 (ATG2 and ATG9) provide phospholipids for the nucleation of autophagosome membranes [38][39][40], which are further matured by the ATG14/beclin1/VPS34 complex [41,42]. ULK1 and beclin1 complexes are positively regulated by the cofactor AMBRA1, which is required for their regulative ubiquitination [43,44]. In mammals, the autophagy conjugation machinery then regulates the lipidation of ATG8 proteins (mATG8) [34,45].…”

Section: Autophagy: An Essential Homeostatic Processmentioning

confidence: 99%

Autophagy and the Lysosomal System in Cancer

Kumar

Sánchez-Álvarez

Lolo

et al. 2021

Cells

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Autophagy and the lysosomal system, together referred to as the autophagolysosomal system, is a cellular quality control network which maintains cellular health and homeostasis by removing cellular waste including protein aggregates, damaged organelles, and invading pathogens. As such, the autophagolysosomal system has roles in a variety of pathophysiological disorders, including cancer, neurological disorders, immune- and inflammation-related diseases, and metabolic alterations, among others. The autophagolysosomal system is controlled by TFEB, a master transcriptional regulator driving the expression of multiple genes, including autophagoly sosomal components. Importantly, Reactive Oxygen Species (ROS) production and control are key aspects of the physiopathological roles of the autophagolysosomal system, and may hold a key for synergistic therapeutic interventions. In this study, we reviewed our current knowledge on the biology and physiopathology of the autophagolysosomal system, and its potential for therapeutic intervention in cancer.

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AMBRA1-regulated autophagy in vertebrate development

Cited by 13 publications

References 99 publications

Autophagy in the Vertebrate Inner Ear

Autophagy in the Vertebrate Inner Ear

Autophagy genes AMBRA1 and ATG8 play key roles in midgut remodeling of the yellow fever mosquito, Aedes aegypti

Autophagy and the Lysosomal System in Cancer

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