Doctoral Researchers

 
Oago Onchuru, Thomas

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JSMC Fellow

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Institute/Dep.
Max Planck Institute for Chemical Ecology
Research Group Insect Symbiosis
PhD Project:

Host and symbiont contributions towards parasite resistance in cotton stainer bugs

 
 
Oetama, Vincensius

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Institute/Dep.
Max Planck Institute for Chemical Ecology
Dept. of Bioorganic Chemistry
PhD Project:

Chlorophyll degradation in Spodoptera littoralis

 
 
Omenge, Keziah

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JSMC Fellow

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Institute/Dep.
Friedrich Schiller University Jena Matthias Schleiden Institute
Chair of Genetics
PhD Project:

‘Reverse zombification’: suppressor mutagenesis of plants overexpressing phytoplasma effector proteins to identify host factors of disease phenotype

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Abstract: Many microbes communicate with plants and animals in intricate ways, which may cause severe diseases. Phytoplasmas are a good case in point. They are cell wall-less eubacteria that...
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... obligatory parasitize and replicate in two very different hosts, plants and transmitting insects. Phytoplasmas occur in plants mainly in phloem tissue and require insects like leafhoppers and psyllids for transmission. Phytoplasmas infect hundreds of plant species, including many important crops, and bring about devastating diseases by causing dramatic symptoms such as phyllody (transformation of floral organs into leaf-like structures), virescence (greening of floral organs) and witches’ broom syndrome (strong increase of the number of stems). Infected plants are often compromised in their reproduction or even sterile; they thus mainly ‘serve’ to reproduce phytoplasmas and hence have been termed “zombie plants”. A cure is not available so far, but sometimes plants are able to recover based on unknown mechanisms. The plant disease phenotypes are caused by effector proteins that are secreted by phytoplasmas, such as SAP11, SAP54 and TENGU of Aster Yellows strain Witches’ Broom (AY-WB). SAP11 leads to the degradation of some CIN-TCP-type transcription factors (CTFs) of the host plant, which inhibits LIPOXYGENASE2 (LOX2) expression and jasmonic acid (JA) biosynthesis, which in turn compromises the plant’s immune system. SAP54 targets MIKC-type MADS-domain transcription factors (MTFs) and mediates their degradation via the ubiquitin/26S proteasome (UPS) pathway. SAP54 may work here like an adapter that links MTFs to RADIATION SENSITIVE23 (RAD23) isoforms RAD23C and RAD23D, which shuttle proteins to the UPS for degradation. Some of the targeted MTFs are part of the ‘floral quartets’ specifying floral organ identity, explaining why SAP54 secretion leads to virescence and phyllody. The target of TENGU is still unknown. Despite recent progress the mechanisms by which phytoplasma effector proteins bring about disease phenotypes are only incompletely known. Importantly, however, expression of single effector proteins of AY-WB in the model plant Arabidopsis thaliana (Arabidopsis) often leads already to the development of almost all the symptoms that characterize a phytoplasma infection. This simplifies experimental approaches aiming at understanding the molecular mechanisms behind the development of disease symptoms. We want to get more detailed insights into the mechanisms by which phytoplasmas manipulate plants. Towards that goal we will identify direct and indirect plant interactors required for the development of disease phenotypes in a comprehensive way, using an unbiased approach. The identification of such plant factors may eventually help to develop methods to attenuate disease phenotypes in crop and ornamental plants.