Talk:MitoEAGLE preprint 2017-09-21

» MitoEAGLE preprint 2017-09-21

Phase 2: Discussion

2017-10-04 MitoEAGLE preprint 2017-09-21 Version 06

• 'Electron transfer system' is changed to 'electron transfer pathways; ETS to ET pathways
• 'Phosphorylation system' is changed to 'phosphorylation pathway'
• 'OXPHOS system' is changed to 'OXPHOS pathway'
• 'ETS capacity' is changed to 'ET capacity' (compare: OXPHOS capacity)
• 'ETS state' is changed to 'ET state' (compare: OXPHOS state)

• 2017-09-27 Asander Frostner E:

• I focused on the sections that I felt are relevant to my level of knowledge. I think it's a very good and educational manuscript, very elaborate and structured. I don't have any input on the contents as such, only a few suggestions on minor text adjustments.

• 2017-09-27 Haavik J:

• I appreciate your efforts to increase the visibility and aid harmonization within this field. I support the initiative and you may well add my name to the growing list of supporters.

• 2017-09-27 Gorr TA:

I added two text sections on pages 10+11 of the manuscript plus references, concerning protein-driven mechanisms of respiration control. Please have a look at the attached pdf and find the two text boxes within the mansucript´s on pp. 10+11. ::::* (6) Regulatory proteins, such as the inhibitory factor 1 (IF1), function in mitochondria of mammals challenged by severe O2 deprivation (hypoxia, anoxia, ischemia) to keep the reversal of proton pumping by complex V (ATP synthase), and, hence, the resulting ATP hydrolysis plus production of reactive oxygen species (ROS), at bay (Matic et al 2016; Esparza-Molto et al. 2017). HIF-1, on the other hand, coordinates access of mitochondrial substrates with hypoxia, in part through the transcriptional activation of the pyruvate dehydrogenase (PDH) inhibitor PDK1. This slow-down of the PDH reaction starves the tricarboxylic acid (TCA) cycle of pyruvate substrate, which, in turn, helps in decreasing respiration rates during conditions of low oxygen availability (Kim et al. 2006, Papandreou et al. 2006). As such, HIF-1 may well contribute in driving the switch from an oxy-regulated to an oxy-conforming mode of respiration (Gnaiger 2003; Gorr 2010; 2017).

• References:

1. Matic I, Cocco S, Ferraina C et al. Neuroprotective coordination of cell mitophagy by the F1Fo-ATPase inhibitory factor (IF1). Pharmacol Research 2016;103:56-68.
2. Esparza-Molto PB, Nuevo-Tapioles C and Cuezva JM. Regulation of the H+-ATP synthase by IF1: a role in mitohormesis. Cell Mol Life Sci 2017;74:2151-66.
3. Kim J-W, Tchernyshyov I, Semenza GL and Dang CV. HIF-1-mediated expression of pyruvate dehydrogenase kinase: A metabolic switch required for cellular adaptation to hypoxia 2006;3:177-85.
4. Papandreou I, Cairns RA, Fontana L, Lim AL and Denko NC. HIF-1 mediates adaptation to hypoxia by actively downregulating mitochondrial oxygen consumption. 2006;3:187-97.
5. Gnaiger E. Oxygen conformance of cellular respiration. A perspective of mitochondrial physiology. 2003;543:39-55.
6. Gorr TA, Wichmann D, Hu J et al. Hypoxia Tolerance in Animals: Biology and Application. Physiol Biochem Zool 2010;83:733-52.
7. Gorr TA. Hypometabolism as the ultimate defence in stress response: how the comparative approach helps understanding of medically relevant questions. Acta Physiol. 2017;219:409-440.

• 2017-09-26 Tomar D:

• I would like to introduce myself as an early career contributor in your excellent work to standardize the nomenclature for mitochondrial bioenergetics. Currently, I am working as a postdoctoral fellow at Temple University, Philadelphia USA and my work focused on the role of calcium in mitochondrial bioenergetics and functions. As a leading author, I discovered the molecular mechanism of one of mitochondrial calcium uniporter regulator (MCUR1) mediated regulation of uniporter function (Cell Reports, 2016). Recently, as a co-first author, I have shown that mitochondrial calcium uniporter senses the reactive oxygen species through the conserved cysteine residue (Molecular Cell, 2017). Besides these contributions in the field of mitochondrial biology, I was the part of the discovery of SPG7 as mitochondrial permeability transition pore from our group (Molecular Cell, 2015) and the association of small RNAs with mitochondria (PlosOne, 2012). I have thoroughly reviewed the preprint of the “The protonmotive force and respiratory control: Building blocks of mitochondrial physiology”. This is an excellent and comprehensive resource for the researchers working in the area of mitochondrial bioenergetics. I have three minor comments on Page 7 and Page 11. I hope these could be useful.

• 2017-09-26 Victor VM:

• Thank you very much for your invitation. I would like to sign the article with you. It is very interesting and accurated article.

• 2017-09-26 MacMillan-Crow LA:

• I think this reads very well. I have made a few comments that might be helpful.

2017-09-24 MitoEAGLE preprint 2017-09-21 Version 04

• 2017-09-23 Robinson MM, Newsom S:

• I reviewed the Preprint of the “Mitochondrial Respiratory Control” joint paper and found it to be quite a useful resource. There are minor editorial updates but overall the main theme and concepts are presented well and I have no major considerations at this point. Thank you for including us in the manuscript as it is very important for standardization of nomenclature.

2017-09-21 MitoEAGLE preprint 2017-09-21 Version 01

Phase 1: Work flow 44 versions until 2017-09-18

» Talk:The protonmotive force and respiratory control