The OXPHOS supercomplex assembly factor HIG2A responds to changes in energetic metabolism and cell cycle

Celia Salazar, Alvaro A. Elorza, Glenda Cofre, Paula Ruiz-Hincapie, Orian Shirihai, Lina María Ruiz

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

HIG2A promotes cell survival under hypoxia and mediates the assembly of complex III and complex IV into respiratory chain supercomplexes. In the present study, we show that human HIGD2A and mouse Higd2a gene expressions are regulated by hypoxia, glucose, and the cell cycle-related transcription factor E2F1. The latter was found to bind the promoter region of HIGD2A. Differential expression of the HIGD2A gene was found in C57BL/6 mice in relation to tissue and age. Besides, the silencing of HIGD2A evidenced the modulation of mitochondrial dynamics proteins namely, OPA1 as a fusion protein increases, while FIS1, a fission protein, decreases. Besides, the mitochondrial membrane potential (ΔΨm) increased. The protein HIG2A is localized in the mitochondria and nucleus. Moreover, we observed that the HIG2A protein interacts with OPA1. Changes in oxygen concentration, glucose availability, and cell cycle regulate HIGD2A expression. Alterations in HIGD2A expression are associated with changes in mitochondrial physiology.

Original languageEnglish
Pages (from-to)17405-17419
Number of pages15
JournalJournal of Cellular Physiology
Volume234
Issue number10
DOIs
Publication statusPublished - 1 Jan 2019

Keywords

  • cell cycle
  • E2F1
  • HIG2A
  • hypoxia
  • mitochondrial dynamics
  • OPA1
  • OXPHOS supercomplexes

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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