Candida albicans PPR proteins are required for the expression of respiratory Complex I subunits

Author:

Wenda Joanna Maria1ORCID,Drzewicka Katarzyna1,Mulica Patrycja1,Tetaud Emmanuel23ORCID,di Rago Jean Paul2,Golik Paweł14ORCID,Łabędzka-Dmoch Karolina1ORCID

Affiliation:

1. Faculty of Biology, Institute of Genetics and Biotechnology, University of Warsaw , Warsaw 02-106 , Poland

2. IBGC, Univ. Bordeaux, CNRS, UMR 5095 , F-33000, Bordeaux , France

3. MFP, Univ. Bordeaux, CNRS, UMR 5234 , F-33000, Bordeaux , France

4. Polish Academy of Sciences, Institute of Biochemistry and Biophysics , Warsaw 00-901 , Poland

Abstract

Abstract Pentatricopeptide repeat (PPR) proteins bind RNA and are present in mitochondria and chloroplasts of Eukaryota. In fungi, they are responsible for controlling mitochondrial genome expression, mainly on the posttranscriptional level. Candida albicans is a human opportunistic pathogen with a facultative anaerobic metabolism which, unlike the model yeast Saccharomyces cerevisiae, possesses mitochondrially encoded respiratory Complex I (CI) subunits and does not tolerate loss of mtDNA. We characterized the function of 4 PPR proteins of C. albicans that lack orthologs in S. cerevisiae and found that they are required for the expression of mitochondrially encoded CI subunits. We demonstrated that these proteins localize to mitochondria and are essential to maintain the respiratory capacity of cells. Deletion of genes encoding these PPR proteins results in changes in steady-state levels of mitochondrial RNAs and proteins. We demonstrated that C. albicans cells lacking CaPpr4, CaPpr11, and CaPpr13 proteins show no CI assembly, whereas the lack of CaPpr7p results in a decreased CI activity. CaPpr13p is required to maintain the bicistronic NAD4L–NAD5 mRNA, whereas the other 3 PPR proteins are likely involved in translation-related assembly of mitochondrially encoded CI subunits. In addition, we show that CaAep3p, which is an ortholog of ScAep3p, performs the evolutionary conserved function of controlling expression of the ATP8–ATP6 mRNA. We also show that C. albicans cells lacking PPR proteins express a higher level of the inducible alternative oxidase (AOX2) which likely rescues respiratory defects and compensates for oxidative stress.

Funder

EU Operational Program Innovative Economy

Foundation for Polish Science

National Science Centre of Poland OPUS

Publisher

Oxford University Press (OUP)

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