bims-cytox1 Biomed news on
Cytochrome oxidase subunit 1
Issue of 2017‒05‒26
three papers selected by
Gavin McStay
New York Institute of Technology


  1. Biochim Biophys Acta. 2017 Sep;doi: 10.1016/j.bbamcr.2017.05.0041864(9):
    Abstract:  Mitochondria are multifunctional metabolic factories and integrative signaling organelles of eukaryotic cells. The structural basis for their numerous functions is a complex and dynamic double-membrane architecture. The outer membrane connects mitochondria to the cytosol and other organelles. The inner membrane is composed of a boundary region and highly folded cristae membranes. The evolutionarily conserved mitochondrial contact site and cristae organizing system (MICOS) connects the two inner membrane domains via formation and stabilization of crista junction structures. Moreover, MICOS establishes contact sites between inner and outer mitochondrial membranes by interacting with outer membrane protein complexes. MICOS deficiency leads to a grossly altered inner membrane architecture resulting in far-reaching functional perturbations in mitochondria. Consequently, mutations affecting the function of MICOS are responsible for a diverse spectrum of human diseases. In this article, we summarize recent insights and concepts on the role of MICOS in the organization of mitochondrial membranes. This article is part of a Special Issue entitled: Membrane Contact Sites edited by Christian Ungermann and Benoit Kornmann.
    Keywords:  Contact sites; Cristae; MICOS; Membrane organization; Mitochondria
  2. Cell Chem Biol. 2017 May 18. doi: 10.1016/j.chembiol.2017.05.01124(5):
    Abstract:  In this issue of Cell Chemical Biology,Wiechmann et al. (2017) identify mitochondrial chaperonin HSP60 as a direct target of myrtucommulone (MC), a nonprenylated acylphloroglucinol that is well known for its apoptotic activity in cancer cells. The authors propose MC as a chemical probe to study HSP60 biology and a potential chemotherapeutic agent in treating cancer and other HSP60-associated diseases.
  3. Int Rev Cell Mol Biol. 2017 ;doi: 10.1016/bs.ircmb.2017.01.001332
    Abstract:  The process of tumorigenesis can be described by a series of molecular features, among which alteration of cellular metabolism has recently emerged. This metabolic rewiring fulfills the energy and biosynthetic demands of fast proliferating cancer cells and amplifies their metabolic repertoire to survive and proliferate in the poorly oxygenated and nutrient-deprived tumor microenvironment. During the last decade, the complex reprogramming of cancer cell metabolism has been widely investigated, revealing cancer-specific metabolic alterations. These include dysregulation of glucose and glutamine metabolism, alterations of lipid synthesis and oxidation, and a complex rewiring of mitochondrial function. However, mitochondria are not the only metabolically active organelles within the cell, and other organelles, including lysosomes, peroxisomes, and endoplasmic reticulum, harbor components of the metabolic network. Of note, dysregulation of the function of these organelles is increasingly recognized in cancer cells. However, to what extent these organelles contribute to the metabolic reprogramming of cancer is not fully understood. In this review, we describe the main metabolic functions of these organelles and provide insights into how they communicate to orchestrate a coordinated metabolic reprogramming during transformation.
    Keywords:  Cancer; Compartmentalization; Metabolic cooperation; Metabolism; Organelle cross talk