Potential mechanisms of CrARF17 on plant defense against periwinkle leaf yellowing phytoplasma

• Main Authors: Leng-Ya Lin, 林稜雅
• Other Authors: 陳仁治
• Format: Others
• Language: en_US
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/09991509876192531417

碩士 === 國立臺灣大學 === 植物病理與微生物學研究所 === 104 === Phytoplasmas are wall-less prokaryotic obligate plant pathogens that are restricted in phloem. These insect-transmittable pathogens cause symptoms including yellows, witches’-broom, virescence, and lead to worldwide economic losses. In periwinkle (Catharanthus roseus), plants may fight against phytoplasmas through systemic acquired resistance (SAR). Previously, we found suppression of CrNPR1, which may play a central role in SAR, result in reduction of CrPR1a induction and acceleration of symptom progression of periwinkle leaf yellowing (PLY), a disease caused by phytoplasma infection. Thus, we hypothesized that transcription factors that can affect the expression of CrPR1a may be involved in plant defense against PLY phytoplasmas and affect symptom progression. Previously, we have screened 307 transcription factors through virus-induced gene silencing (VIGS) and identified factors that regulate CrPR1a expression. These factors include three ARFs, one Aux/IAA, and one bZIP family members. In this proposed study, we aimed to understand whether these transcription factors are direct or indirectly involved in plant defense against PLY phytoplasma. In two preliminary tests, silencing of an Arabidopsis ARF17 ortholog, CrARF17, not only reduced the expression of CrPR1a, but also accelerated disease progression of PLY. The result is consistent with previous finding that silencing of CrARF17 resulted in repression of CrPR1a induction. Studies in Arabidopsis have shown that ARFs participate in auxin signaling and auxin can affect plant resistance through repressing of salicylic acid (SA) biosynthesis. In this study, we have clarified that silencing of CrARF17 resulted in increase of GH3 gene expression and repression of SA, IAA and IAA-Asp accumulation. Then, GH3 and most of CalS genes are induced in plants after PLY infection. We speculate that CrARF17 participates in plant resistance indirectly against PLY phytoplasmas. In the future, we will focus on clarifying the role of GH3 and CalS genes in plant resistance to PLY, and further clarify the effect of callose accumulation and the IAA-Asp level on symptom progression of PLY.