Disruption of ppr3, ppr4, ppr6 or ppr10 induces flocculation and filamentous growth in Schizosaccharomyces pombe.

Abstract

Pentatricopeptide repeat (PPR) proteins are major players in mitochondrial and chloroplast RNA metabolism, which is essential for normal organellar function. The fission yeast Schizosaccharomyces pombe has 10 PPR proteins. We have previously reported that loss of ppr3, ppr4, ppr6 or ppr10 perturbs iron homeostasis leading to accumulation of reactive oxygen species and apoptotic cell death. In the present study, we show that loss of ppr3, ppr4, ppr6 or ppr10 can cause non-sexual flocculation and filamentous growth of cells. Furthermore, expression of a number of genes encoding cell-surface flocculins and cell wall-remodeling enzymes are induced in these ppr-deletion mutants. We also show that Δppr10 cells, and, to a lesser extent, Δppr4 and Δppr6 cells, exhibited increased tolerance to H2O2 toxicity compared with the wild-type strain. Finally, we found that overexpression of genes involved in iron uptake and/or iron homeostasis could cause the flocculation of wild-type cells. Our findings suggest that an elevated level of intracellular iron in the mutant caused by loss of ppr3, ppr4, ppr6 or ppr10 may result in flocculation and filamentous growth in S. pombe.