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Title: Ultraviolet irradiation alters the density of inner mitochondrial membrane and proportion of inter-mitochondrial junctions in copepod myocytes
Award ID(s):
1736150 1453784
Author(s) / Creator(s):
; ; ;
Date Published:
Journal Name:
Page Range / eLocation ID:
82 to 90
Medium: X
Sponsoring Org:
National Science Foundation
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  1. Abstract

    Recent publications report that although the mitochondria population in an axon can be quickly replaced by a combination of retrograde and anterograde axonal transport (often within less than 24 hours), the axon contains much older mitochondria. This suggests that not all mitochondria that reach the soma are degraded and that some are recirculating back into the axon. To explain this, we developed a model that simulates mitochondria distribution when a portion of mitochondria that return to the soma are redirected back to the axon rather than being destroyed in somatic lysosomes. Utilizing the developed model, we studied how the percentage of returning mitochondria affects the mean age and age density distributions of mitochondria at different distances from the soma. We also investigated whether turning off the mitochondrial anchoring switch can reduce the mean age of mitochondria. For this purpose, we studied the effect of reducing the value of a parameter that characterizes the probability of mitochondria transition to the stationary (anchored) state. The reduction in mitochondria mean age observed when the anchoring probability is reduced suggests that some injured neurons may be saved if the percentage of stationary mitochondria is decreased. The replacement of possibly damaged stationary mitochondria with newly synthesized ones may restore the energy supply in an injured axon. We also performed a sensitivity study of the mean age of stationary mitochondria to the parameter that determines what portion of mitochondria re‐enter the axon and the parameter that determines the probability of mitochondria transition to the stationary state. The sensitivity of the mean age of stationary mitochondria to the mitochondria stopping probability increases linearly with the number of compartments in the axon. High stopping probability in long axons can significantly increase mitochondrial age.

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  2. Abstract

    Numerous age‐related human diseases have been associated with deficiencies in cellular energy production. Moreover, genetic alterations resulting in mitochondrial dysfunction are the cause of inheritable disorders commonly known as mitochondrial diseases. Many of these deficiencies have been directly or indirectly linked to deficits in mitochondrial gene expression. Transcription is an essential step in gene expression and elucidating the molecular mechanisms involved in this process is critical for understanding defects in energy production. For the past five decades, substantial efforts have been invested in the field of mitochondrial transcription. These efforts have led to the discovery of the main protein factors responsible for transcription as well as to a basic mechanistic understanding of the transcription process. They have also revealed various mechanisms of transcriptional regulation as well as the links that exist between the transcription process and downstream processes of RNA maturation. Here, we review the knowledge gathered in early mitochondrial transcription studies and focus on recent findings that shape our current understanding of mitochondrial transcription, posttranscriptional processing, as well as transcriptional regulation in mammalian systems.

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    The mitonuclear species concept hypothesizes that incompatibilities between interacting gene products of the nuclear and mitochondrial genomes are a major factor establishing and maintaining species boundaries. However, most of the data available to test this concept come from studies of genetic variation in mitochondrial DNA, and clines in the mitochondrial genome across contact zones can be produced by a variety of forces. Here, we show that using a combination of population genomic analyses of the nuclear and mitochondrial genomes and studies of mitochondrial function can provide insight into the relative roles of neutral processes, adaptive evolution, and mitonuclear incompatibility in establishing and maintaining mitochondrial clines, using Atlantic killifish (Fundulus heteroclitus) as a case study. There is strong evidence for a role of secondary contact following the last glaciation in shaping a steep mitochondrial cline across a contact zone between northern and southern subspecies of killifish, but there is also evidence for a role of adaptive evolution in driving differentiation between the subspecies in a variety of traits from the level of the whole organism to the level of mitochondrial function. In addition, studies are beginning to address the potential for mitonuclear incompatibilities in admixed populations. However, population genomic studies have failed to detect evidence for a strong and pervasive influence of mitonuclear incompatibilities, and we suggest that polygenic selection may be responsible for the complex patterns observed. This case study demonstrates that multiple forces can act together in shaping mitochondrial clines, and illustrates the challenge of disentangling their relative roles.

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