Mouse lymphomyeloid cells can function with significantly decreased expression levels of cytochrome C

Biochemistry (Mosc). 2014 Dec;79(12):1412-22. doi: 10.1134/S0006297914120177.

Abstract

Cytochrome c is an indispensable electron carrier in the mitochondrial respiratory chain and also an important mediator of the internal pathway triggering apoptosis. Mice with a complete deficiency of the Cycs gene encoding the somatic cytochrome c die during the embryogenesis. Using the technology of LoxP-cre-dependent tissue-specific recombination, we obtained some mouse strains with significantly reduced expression of cytochrome c in certain cell types ("conditional genetic knockdown"). This knockdown was achieved by abrogation of the normal splicing of the Cycs locus pre-mRNA due to an additional acceptor site inside the stop-cassette neo(r). Previously, we observed embryonic lethality in homozygous mice with the same knockdown of cytochrome c in all cells of the organism. In the present work we studied two novel mouse strains with conditional knockdown of the Cycs gene in T lymphocytes and macrophages. Somewhat surprisingly, the mice of these two strains under normal conditions were not phenotypically different from the wild-type mice, either on the whole organism level or on the level of activity of individual target cells. Thus, the amount of cytochrome c in lymphomyeloid cells does not affect their development and normal functioning.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cytochromes c / deficiency
  • Cytochromes c / genetics*
  • Exons / genetics
  • Gene Expression Regulation, Enzymologic*
  • Gene Knockdown Techniques
  • Macrophages / cytology
  • Macrophages / enzymology*
  • Mice
  • Molecular Sequence Data
  • T-Lymphocytes / cytology
  • T-Lymphocytes / enzymology*

Substances

  • Cytochromes c