ISHS Acta Horticulturae 1010: III International Humulus Symposium
HOP STUNT VIROID PATHOGENESIS INVOLVES A DISBALANCE OF HOP REGULATORY GENES |
| Authors: | Z. Füssy, J. Matousek, J. Patzak, G. Steger , K. Uhlírová |
| Keywords: | gene expression, transcription factor, Humulus lupulus L., phenylpropanoid, Real Time quantitative RT-PCR |
| DOI: | 10.17660/ActaHortic.2013.1010.13 |
| Abstract:
Hop stunt viroid (HpSVd) is a serious pathogen with symptoms ranging from metabolic to developmental changes. In hop Humulus lupulus ‘Admiral’ infected with HpSVd-g we observed stunted growth, leaf rugosity and epinasty, and petiole decolouration, along with detected shifts in secondary metabolite levels. Owing to simple structure, HpSVd is hypothesised to exert symptoms via viroid-derived small RNA species and subsequent transcriptional silencing mechanisms. In search of genes linked with the disease, we employed quantitative expression screening of authentic hop transcription factors (TFs), as well as newly identified genes, including ones predicted to be directly targeted by certain vd-sRNAs. The most profound changes were detected in HlWRKY1, HlMyb3, and RSP13, with increased mRNA levels, while HlbHLH1, HlbHLH2, HlbZIP1, DEADc, DRL1, and HlMyb4 mRNA levels were markedly decreased. The precise effect of these changes still needs to be revealed. However, HlMyb3 and HlbHLH2 were recently shown to co-operate in regulation of chalcon synthase chs_H1 gene encoding a flavonoid pathway key enzyme (Matoušek et al., 2012a). Solely the disbalance of these transcription factors influences the flux through flavonoid pathways, having biotechnological potential for future research. In addition, bioinformatic prediction of HpSVd-derived small RNA targets identified chs_H1 mRNA as effective target. Marked decrease of its expression was confirmed in diseased samples, and some interaction with HpSVd takes place also in a host weed, Galinsoga ciliate, as determined by transient co-expression. The unveiling of the precise mechanism is still in progress. TF disbalance may therefore combine with direct chs_H1 mRNA degradation to induce secondary metabolite-related symptoms. | |
Download Adobe Acrobat Reader (free software to read PDF files) | |
