Tracking Mitochondrial Density and Positioning along a Growing Neuronal Process in Individual<i>C. elegans</i>Neuron Using a Long-Term Growth and Imaging Microfluidic Device

Mondal, Sudip; Dubey, Jyoti; Awasthi, Anjali; Sure, Guruprasad Reddy; Vasudevan, Amruta; Koushika, Sandhya P.

doi:10.1523/eneuro.0360-20.2021

Cited by 8 publications

(5 citation statements)

References 76 publications

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“…The uniform distribution displayed in Figure S1a is consistent with Reference 40 which noted that in axons the mitochondrial density is independent of the distance from the soma (Figure 1C in Reference 40). A constant mitochondrial density of 5 mitochondria/100 μm was also reported for growing neuronal processes in C. elegans 41 …”

Section: Resultssupporting

confidence: 56%

“…A constant mitochondrial density of 5 mitochondria/100 μm was also reported for growing neuronal processes in C. elegans. 41 The return of 30% (α ¼ 0:3, p s ¼ 0:4) of exiting mitochondria back to the axon results in the same uniform distribution of mitochondria along the axon length (Figure S1a). This is because we assumed that the total flux of mitochondria entering the first demand site is the same for all cases computed in this paper.…”

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confidence: 84%

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Effect of mitochondrial circulation on mitochondrial age density distribution

Kuznetsov,

Kuznetsov

2023

Numer Methods Biomed Eng

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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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Section: Resultssupporting

confidence: 56%

mentioning

confidence: 84%

Effect of mitochondrial circulation on mitochondrial age density distribution

Kuznetsov,

Kuznetsov

2023

Numer Methods Biomed Eng

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“…[34]). A constant mitochondrial density of 5 mitochondria/100 μm was also reported for growing neuronal processes in C. elegans [35].…”

Section: Resultsmentioning

confidence: 62%

Effect of mitochondrial circulation on mitochondrial age density distribution

Кузнецов

2022

Preprint

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Recent publications report that although mitochondria population in an axon can be quickly replaced by combination of retrograde and anterograde axonal transport (often within less than 24 h), the axon contains much older mitochondria. This suggests that not all mitochondria that reach the soma are degraded, some of them participate in recirculation. To explain this we developed a model that simulates that 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 mitochondria 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 of the mean age of mitochondria observed when the chance of mitochondria to get anchored is reduced suggests that some injured neurons may be saved if the percentage of stationary mitochondria is decreased. Replacement of possibly damaged stationary mitochondria with newly synthesized ones may restore 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.

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“…Parenthetically, we did not test the possibility that mitochondria determine the distribution of varicosities (or synapses) as synapses and varicosities are stable on time scales over which mitochondria traverse long distances along these neuronal processes (Morsci et al, 2016; Mondal et al, 2021). We defined varicosities as swellings bounded on both sides by restrictions in neuronal diameter of at least 30% (Fig.…”

Section: Resultsmentioning

confidence: 99%

Ultrastructural analysis reveals mitochondrial placement independent of synapse placement in fine caliber C. elegans neurons

Riboul,

Crill,

Oliva

et al. 2023

Preprint

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Neurons rely on mitochondria for an efficient supply of ATP and other metabolites. However, while neurons are highly elongated, mitochondria are discrete and limited in number. Due to the slow rates of diffusion of long distances it follows that neurons would benefit from an ability to control the distribution of mitochondria to sites of high metabolic activity, such as synapses. It is assumed that neurons possess this capacity, but ultrastructural data over substantial portions of a neurons extent that would allow for tests of such hypotheses are scarce. Here, we mined the Caenorhabditis elegans electron micrographs of John White and Sydney Brenner and found systematic differences in average mitochondrial size (ranging from 1.4 to 2.6 microns), volume density (3.8% to 7.1%) and diameter (0.19 to 0.25 microns) between neurons of different neurotransmitter type and function, but found no differences in mitochondrial morphometrics between axons and dendrites of the same neurons. Analyses of distance intervals found mitochondria to be distributed randomly with respect to both presynaptic and postsynaptic specializations. Presynaptic specializations were primarily localized to varicosities, but mitochondria were no more likely to be found in synaptic varicosities than non-synaptic varicosities. Consistently, mitochondrial volume density was no greater in varicosities with synapses. Therefore, beyond the capacity to disperse mitochondria throughout their length, at least in C. elegans, fine caliber neurons manifest little in the way of subcellular control of mitochondria.

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Tracking Mitochondrial Density and Positioning along a Growing Neuronal Process in IndividualC. elegansNeuron Using a Long-Term Growth and Imaging Microfluidic Device

Abstract: Tracking mitochondrial density and positioning along a growing neuronal process in individual C. elegans neuron using a long-term growth and imaging microfluidic device

Cited by 8 publications

References 76 publications

Effect of mitochondrial circulation on mitochondrial age density distribution

Effect of mitochondrial circulation on mitochondrial age density distribution

Effect of mitochondrial circulation on mitochondrial age density distribution

Ultrastructural analysis reveals mitochondrial placement independent of synapse placement in fine caliber C. elegans neurons

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