How do yeast sense mitochondrial dysfunction?

Authors:

Dmitry A. Knorre1, Svyatoslav S. Sokolov1, Anna N. Zyrina2, Fedor F. Severin1,3

doi: 10.15698/mic2016.11.537
Volume 3, pp. 532 to 539, published 22/09/2016.

Affiliations:

1 Belozersky Institute of Physico-Chemical Biology, Moscow State University, Leninskiye Gory 1-40, Moscow 119991, Russia.

2 Faculty of Bioengineering and Bioinformatics, Moscow State University, Leninskiye Gory 1-73, Moscow 119991, Russia.

3 Institute of Mitoengineering, Moscow State University, Leninskiye Gory 1, Moscow 119991, Russia.

Keywords: 

mitochondria, yeast, retrograde signaling, ROS.

Corresponding Author(s):

Fedor F. Severin, severin@belozersky.msu.ru

Conflict of interest statement:

The authors declare no conflict of interest.

Please cite this article as:

Dmitry A. Knorre, Svyatoslav S. Sokolov, Anna N. Zyrina, Fedor F. Severin (2016). How do yeast sense mitochondrial dysfunction? Microbial Cell 3(11): 532-539. doi: 10.15698/mic2016.11.537

© 2016 Knorre et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

Apart from energy transformation, mitochondria play important signaling roles. In yeast, mitochondrial signaling relies on several molecular cascades. However, it is not clear how a cell detects a particular mitochondrial malfunction. The problem is that there are many possible manifestations of mitochondrial dysfunction. For example, exposure to the specific antibiotics can either decrease (inhibitors of respiratory chain) or increase (inhibitors of ATP-synthase) mitochondrial transmembrane potential. Moreover, even in the absence of the dysfunctions, a cell needs feedback from mitochondria to coordinate mitochondrial biogenesis and/or removal by mitophagy during the division cycle. To cope with the complexity, only a limited set of compounds is monitored by yeast cells to estimate mitochondrial functionality. The known examples of such compounds are ATP, reactive oxygen species, intermediates of amino acids synthesis, short peptides, Fe-S clusters and heme, and also the precursor proteins which fail to be imported by mitochondria. On one hand, the levels of these molecules depend not only on mitochondria. On the other hand, these substances are recognized by the cytosolic sensors which transmit the signals to the nucleus leading to general, as opposed to mitochondria-specific, transcriptional response. Therefore, we argue that both ways of mitochondria-to-nucleus communication in yeast are mostly (if not completely) unspecific, are mediated by the cytosolic signaling machinery and strongly depend on cellular metabolic state.