Viroid Research

Viroids are the smallest known pathogens. They consist of circular-closed RNA molecules and infest only plants. Viroids do not code for proteins. They require the enzymes of their hosts for their replication, processing and systemic expansion. Similar to viral infections, viroid infections also activate RNA interference (RNAi), as evidenced by the detection of viroid-generated siRNAs (vd-siRNAs). Viroids do not produce silencing suppressor proteins and must therefore have developed an alternative strategy to protect themselves from degradation of their RNA by the cytoplasmic RNAi. Their replication in the nucleus (Pospiviroidae) or in the chloroplasts (Avsunviroidae) may contribute to this protection strategy. However, in order to be able to systemically infect a plant, viroids must leave their replication site and move through the cytoplasm into neighboring cells. Due to the high degree of self-complementarity, viroid RNA can form a rod-shaped secondary structure, which probably impairs the attack of the RNAi machinery. In the context of viroid research, we therefore do not only want to diagnose viroid infections (Services), but we also want to find out whether viroids have developed further protective mechanisms against RNAi, and how viroids affect the fitness of their host plants.

 current Projects

Viroid-induced symptom expression in tomato
In-house funding

Transcriptome data of potato spindle tuber viroid (PSTVd) -infected tomatoes show that hundreds of genes are deregulated compared to viroid-free tomatoes. It is postulated that vd-siRNAs, which, in the case of a viroid infection, accumulate in large quantities in plant cells, lead to the inactivation of endogenes. We are therefore investigating whether candidate genes whose transcripts have high complementarity with vd-siRNAs are down-regulated in PSTVd-infected tomatoes.

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