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RNA Biology in Fungal Phytopathogens

PLoS Pathogens
Public Library of Science
Publication Date
DOI: 10.1371/journal.ppat.1003617
  • Pearls
  • Biology
  • Medicine


ppat.1003617 1..3 Pearls RNA Biology in Fungal Phytopathogens Vera Go¨hre, Carl Haag, Michael Feldbru¨gge* Heinrich-Heine University Du¨sseldorf, Institute for Microbiology, Cluster of Excellence on Plant Sciences, Du¨sseldorf, Germany RNA-dependent processes are essential to determine when, where, and how much of a protein is synthesized. In eukaryotes, these processes start with transcription in the nucleus and end with mRNA translation at distinct cytoplasmic sites followed by mRNA degradation [1]. In between, a number of defined steps occur such as 59 capping, splicing, polyadenylation, nuclear export, and cytoplasmic transport. Most of the steps are tightly regulated to achieve highly precise spatiotemporal expression. RNA-binding proteins serve as key factors that are essential at each level of posttranscriptional control [1]. Small RNAs are additional factors that can inhibit translation or are able to promote degradation of mRNAs. Due to the central importance of RNA biology in regulating protein synthesis, it is not surprising that fungal pathogens intensely rely on RNA-dependent processes to control infection. Here, we focus on RNA biology in fungal plant pathogenesis, which is best studied in the corn smut Ustilago maydis [2,3]. RNA Biology Orchestrates Fungal Infection In U. maydis, a major pathogenicity determinant is the homeodomain transcription factor bW/bE that triggers a cascade of transcriptional responses essential for full virulence [4,5]. Progression toward infection is regulated by several bE/bW- induced factors, including Clp1 and Cib1. Importantly, their functions are precisely regulated at the posttranscriptional level. clp1 is a direct target gene of bW/bE, which is induced early during formation of infectious filaments. However, the Clp1 protein is only synthesized later at the specific stage of plant penetration when it acts as an antagonist of bW/bE [6]. This is indicative for a tight translational regulation

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