Location: Molecular Plant Pathology LaboratoryTitle: Pathological modifications of plant stem cell destiny
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 8/15/2015
Publication Date: 8/18/2015
Citation: Wei, W., Davis, R.E., Zhao, Y. 2015. Pathological modifications of plant stem cell destiny. Meeting Abstract. 2015 Mid-Atlantic Plant Molecular Biology Society Meeting.
Technical Abstract: In higher plants, the shoot apex contains undifferentiated stem cells that give rise to various tissues and organs. The fate of these stem cells determines the pattern of plant growth as well as reproduction; and such fate is genetically preprogrammed. We found that a bacterial infection can derail plant stem cells from their genetically preprogrammed destiny, therefore altering the pattern of growth and development of the plant. Using the Columbia Basin potato purple top (PPT) phytoplasma and its alternative host tomato as a model system, we identified several mutually distinct symptoms exhibited by infected plants, and found that each symptom type corresponds to a distinct phase in modification of stem cell destiny. Such stem cell destiny modifications include premature floral meristem termination, suppressed floral meristem initiation, delayed vegetative-to-inflorescence meristem conversion, and repetitive initiation of lateral vegetative meristems. Our results revealed that transcriptional reprogramming of key meristem switching genes occurred prior to symptom appearance. Based on these findings, we hypothesized that reprogramming of stem cell fate represents the unifying mechanism that underlies phytoplasmal disease symptoms that manifested alterations of plant architecture and morphology. In testing our hypothesis in the present study, we identified additional symptoms in PPT phytoplasma-infected tomato plants, and determined expression profiles of an array of meristem switching genes in relation to the emergence and development of these symptoms. Our findings advance understanding of plant growth and development under both normal and pathological conditions, and elucidate the coupling of altered gene expression and modified meristerm fate giving rise to abnormal organogenesis, the hallmark of phytoplasmal infection.