By Eliana Y. L. Chan, Jarungjit Rujiviphat (auth.), Bingwei Lu (eds.)
Mitochondria are crucial organelles in eukaryotic cells that keep watch over such assorted strategies as power metabolism, calcium buffering, and phone demise. contemporary stories have printed that adjustments in mitochondrial morphology by means of fission and fusion, a method often called mitochondrial dynamics, is very vital for the functionality and survival of neurons. Defects during this strategy are generally present in neurodegenerative illnesses, delivering a brand new paradigm for investigating mechanisms of neurodegeneration.
This is the 1st ebook that integrates in a single quantity such varied topics because the genetic regulate of mitochondrial dynamics, the connection among mitochondrial dynamics and bioenergetics, the jobs of mitochondrial dynamics in apoptosis, axonal shipping, mitochondrial quality controls, and the contribution of faulty mitochondrial dynamics to the pathogenesis of neurodegenerative diseases.
Focusing on mitochondrial dynamics and its position in neurodegeneration, this bookbrings jointly 32 top scientists and clinicians from worldwide to carry a entire treatise on all elements of mitochondrial dynamics, from simple study on its molecular foundation to its clinical implications. The authors have contributed cutting-edge chapters on their respective parts of craftsmanship, offering readers attracted to mitochondrial biology and mechanisms of neurodegenerative ailments with the freshest information.
This absolutely illustrated volume
• offers a complete historic account of discoveries resulting in the identity of key molecular gamers all in favour of mitochondrial dynamics, emphasizing the function performed via version organism genetics.
• Describes the basic mechanisms during which mitochondrial dynamics and mobile strength prestige can reciprocally control each one other.
• Discusses the legislation and inter-dependence of mitochondrial dynamics and mitochondrial autophagy (mitophagy) in mitochondrial caliber control.
• Highlights the significance of mitochondrial dynamics within the well timed execution of apoptosis.
• info the molecular techniques that bring about the delivery and distribution of mitochondria to neuronal axons and synapses, arguably essentially the most vital elements of neuronal physiology
• provides fresh findings at the scientific range of illnesses because of mutations within the mitochondrial dynamics equipment, the spectrum of mutations within the mitochondrial fusion genes and the corresponding pathophysiology, and the healing perspectives.
• Summarizes a speedily growing to be physique of literature targeting the position of mitochondrial dynamics within the pathogenesis of Parkinson’s affliction and discusses unresolved controversies within the box within the context of a dynamic community of compensatory responses to mitochondrial pressure, disorder and injury.
• Highlights the position of aberrant mitochondrial dynamics within the pathogenesis of Alzheimer’s affliction, and provides a molecular mechanism connecting disease-causing insults and post-translational amendment of the mitochondrial fission machinery.
• Discusses the printed literature linking mitochondrial disorder in Huntington’s affliction, concentrating on the position that defects in mitochondrial dynamics could play in ailment pathogenesis.
Professor Lu has summarized the issues linked to the nascent yet swiftly becoming examine box of mitochondrial dynamics in neurodegeneration and has been profitable in modifying a must-read e-book for college students, clinicians, and researchers drawn to mitochondria biology, neurobiology, and mechanisms of neurodegenerative diseases.
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Extra info for Mitochondrial Dynamics and Neurodegeneration
2009). Although desumoylation during the G2/M transition increases fission, steady state desumoylation of Drp1 promoted mitochondrial elongation (Zunino et al. 2007, 2009). These data underscore the importance of this post-translational modification, and it is likely that several other factors undergo sumoylation to regulate mitochondrial division in the different contexts during the life of the cell. 2 Ubiquitination It is becoming increasingly clear that ubiquitination is a key regulator of mitochondrial function.
2 Inner Membrane Fusion Mechanistic Model of Inner Membrane Fusion Mgm1/OPA1 Mgm1 was first identified in a screen for genes involved in mitochondrial genome maintenance. Mutations in MGM1 caused temperature-sensitive loss of mtDNA (Jones and Fangman 1992). Mgm1 was later shown to play a role in mitochondrial 1 The Genetics of Mitochondrial Fusion and Fission 27 fusion and subsequently shown to be a key mediator of inner membrane fusion. Deletion and mutations in MGM1 were shown to result in fragmented mitochondria and impaired mitochondrial fusion during mating that could be rescued by a DNM1 deletion (Wong et al.
2010). 1). In support of this idea, studies show that only transient but not complete mitochondrial fusion was observed in OPA1 knock-down or over-expressing cells (Liu et al. 2009), and mitochondria with abnormal shape have a reduced ability to fuse to normal ones (Navratil et al. 2008). 3 Roles in Quality Control Systems Mitophagy and apoptosis are quality control mechanisms at organellar and cellular levels, respectively. Mitophagy is a mechanism by which severely damaged mitochondria are degraded to prevent them from fusing and sharing toxic material with other mitochondria in the network (discussed in more detail below).