Deciphering Effector Protein Functions of Ustilago maydis involved in gall formation
Deciphering Effector Protein Functions of Ustilago maydis involved in gall formation
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DissertationDate of Exam
22.03.2024Date of Publication
14.06.2024Advisor
Djamei, ArminCo-Referee
Dörmann, PeterMetadata
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Abstract
Plants are location-bound organisms and thus directly exposed to their environmental conditions. Unlike mammals, plants lack a somatic adaptive immune system and therefore need to rely on their innate immune system and the activation of diverse signaling pathways emerging from the infected region. Plants have developed intricate defense mechanisms to identify and respond to invaders. To achieve a successful infection, plant invaders pathogens, require strategies to suppress defense responses and manipulate metabolic processes. For this purpose, pathogens secrete molecules called effectors in order to loot nutrients necessary for their growth and reproduction. This ongoing competition between the pathogen and the host revolves around gaining new effectors and defense proteins, respectively.
Cereal grains meet nearly half of humankind's caloric requirement. Wheat, maize, and rice are humans’ most common food resources. Maize is the most preferred grain in southern and Eastern Africa, Central America, and Mexico. The biotrophic fungus Ustilago maydis causes smut disease in maize (Z. mays) and teosinte (Z. mays ssp. parviglumis). U. maydis is an outstanding model organism for studying various aspects of plant-pathogen interactions. U. maydis promotes the formation of galls in all aerial parts of the host plant, in contrast to other smut fungi such as Ustilago hordei, Tilletia caries, Tilletia laevis.
In the presented study, I mostly worked on a U. maydis effector that was genetically located in cluster 5A. The effector called cabbage-like phenotype 1 (Cab1) is based on the observed phenotype of over-expression in the non-host system, A. thaliana. I could demonstrate that Cab1 targets BIN2 (Shaggy-like kinase 3) at the C-terminal domain and re-localizes BIN2 from the cytosol to the nucleus. In the results of Cab1-Bin2 interaction in the non-host system, I showed 10 times more phosphorylation of AtBIN2 Tyrosine Y200, and five times less ubiquitination of AtBIN2-Lysine35 than the control. Respectively, these post-translation modifications correlate to higher activity and less degradation of AtBin2 in the presence of Cab1. The results of total RNA sequencing showed that Cab1 induction downregulates Samll Auxin Up-regulated RNAs (SAURs) and Expansins (EXPs)-mediated cell wall expansion which also aligns with our phenotypic observations and molecular studies. I showed the Cab1 mechanism to promote the AtBin2 active state in planta. The appendix contains my contributions to other unpublished studies in the lab during my Ph.D. career at Djamei lab.
Cereal grains meet nearly half of humankind's caloric requirement. Wheat, maize, and rice are humans’ most common food resources. Maize is the most preferred grain in southern and Eastern Africa, Central America, and Mexico. The biotrophic fungus Ustilago maydis causes smut disease in maize (Z. mays) and teosinte (Z. mays ssp. parviglumis). U. maydis is an outstanding model organism for studying various aspects of plant-pathogen interactions. U. maydis promotes the formation of galls in all aerial parts of the host plant, in contrast to other smut fungi such as Ustilago hordei, Tilletia caries, Tilletia laevis.
In the presented study, I mostly worked on a U. maydis effector that was genetically located in cluster 5A. The effector called cabbage-like phenotype 1 (Cab1) is based on the observed phenotype of over-expression in the non-host system, A. thaliana. I could demonstrate that Cab1 targets BIN2 (Shaggy-like kinase 3) at the C-terminal domain and re-localizes BIN2 from the cytosol to the nucleus. In the results of Cab1-Bin2 interaction in the non-host system, I showed 10 times more phosphorylation of AtBIN2 Tyrosine Y200, and five times less ubiquitination of AtBIN2-Lysine35 than the control. Respectively, these post-translation modifications correlate to higher activity and less degradation of AtBin2 in the presence of Cab1. The results of total RNA sequencing showed that Cab1 induction downregulates Samll Auxin Up-regulated RNAs (SAURs) and Expansins (EXPs)-mediated cell wall expansion which also aligns with our phenotypic observations and molecular studies. I showed the Cab1 mechanism to promote the AtBin2 active state in planta. The appendix contains my contributions to other unpublished studies in the lab during my Ph.D. career at Djamei lab.
Classification (DDC)
570 Biowissenschaften, BiologieBahrami, Pouria: Deciphering Effector Protein Functions of Ustilago maydis involved in gall formation. - Bonn, 2024. - Dissertation, Rheinische Friedrich-Wilhelms-Universität Bonn.
Online-Ausgabe in bonndoc: https://nbn-resolving.org/urn:nbn:de:hbz:5-76287
Online-Ausgabe in bonndoc: https://nbn-resolving.org/urn:nbn:de:hbz:5-76287
@phdthesis{handle:20.500.11811/11602,
urn: https://nbn-resolving.org/urn:nbn:de:hbz:5-76287,
author = {{Pouria Bahrami}},
title = {Deciphering Effector Protein Functions of Ustilago maydis involved in gall formation},
school = {Rheinische Friedrich-Wilhelms-Universität Bonn},
year = 2024,
month = jun,
note = {Plants are location-bound organisms and thus directly exposed to their environmental conditions. Unlike mammals, plants lack a somatic adaptive immune system and therefore need to rely on their innate immune system and the activation of diverse signaling pathways emerging from the infected region. Plants have developed intricate defense mechanisms to identify and respond to invaders. To achieve a successful infection, plant invaders pathogens, require strategies to suppress defense responses and manipulate metabolic processes. For this purpose, pathogens secrete molecules called effectors in order to loot nutrients necessary for their growth and reproduction. This ongoing competition between the pathogen and the host revolves around gaining new effectors and defense proteins, respectively.
Cereal grains meet nearly half of humankind's caloric requirement. Wheat, maize, and rice are humans’ most common food resources. Maize is the most preferred grain in southern and Eastern Africa, Central America, and Mexico. The biotrophic fungus Ustilago maydis causes smut disease in maize (Z. mays) and teosinte (Z. mays ssp. parviglumis). U. maydis is an outstanding model organism for studying various aspects of plant-pathogen interactions. U. maydis promotes the formation of galls in all aerial parts of the host plant, in contrast to other smut fungi such as Ustilago hordei, Tilletia caries, Tilletia laevis.
In the presented study, I mostly worked on a U. maydis effector that was genetically located in cluster 5A. The effector called cabbage-like phenotype 1 (Cab1) is based on the observed phenotype of over-expression in the non-host system, A. thaliana. I could demonstrate that Cab1 targets BIN2 (Shaggy-like kinase 3) at the C-terminal domain and re-localizes BIN2 from the cytosol to the nucleus. In the results of Cab1-Bin2 interaction in the non-host system, I showed 10 times more phosphorylation of AtBIN2 Tyrosine Y200, and five times less ubiquitination of AtBIN2-Lysine35 than the control. Respectively, these post-translation modifications correlate to higher activity and less degradation of AtBin2 in the presence of Cab1. The results of total RNA sequencing showed that Cab1 induction downregulates Samll Auxin Up-regulated RNAs (SAURs) and Expansins (EXPs)-mediated cell wall expansion which also aligns with our phenotypic observations and molecular studies. I showed the Cab1 mechanism to promote the AtBin2 active state in planta. The appendix contains my contributions to other unpublished studies in the lab during my Ph.D. career at Djamei lab.},
url = {https://hdl.handle.net/20.500.11811/11602}
}
urn: https://nbn-resolving.org/urn:nbn:de:hbz:5-76287,
author = {{Pouria Bahrami}},
title = {Deciphering Effector Protein Functions of Ustilago maydis involved in gall formation},
school = {Rheinische Friedrich-Wilhelms-Universität Bonn},
year = 2024,
month = jun,
note = {Plants are location-bound organisms and thus directly exposed to their environmental conditions. Unlike mammals, plants lack a somatic adaptive immune system and therefore need to rely on their innate immune system and the activation of diverse signaling pathways emerging from the infected region. Plants have developed intricate defense mechanisms to identify and respond to invaders. To achieve a successful infection, plant invaders pathogens, require strategies to suppress defense responses and manipulate metabolic processes. For this purpose, pathogens secrete molecules called effectors in order to loot nutrients necessary for their growth and reproduction. This ongoing competition between the pathogen and the host revolves around gaining new effectors and defense proteins, respectively.
Cereal grains meet nearly half of humankind's caloric requirement. Wheat, maize, and rice are humans’ most common food resources. Maize is the most preferred grain in southern and Eastern Africa, Central America, and Mexico. The biotrophic fungus Ustilago maydis causes smut disease in maize (Z. mays) and teosinte (Z. mays ssp. parviglumis). U. maydis is an outstanding model organism for studying various aspects of plant-pathogen interactions. U. maydis promotes the formation of galls in all aerial parts of the host plant, in contrast to other smut fungi such as Ustilago hordei, Tilletia caries, Tilletia laevis.
In the presented study, I mostly worked on a U. maydis effector that was genetically located in cluster 5A. The effector called cabbage-like phenotype 1 (Cab1) is based on the observed phenotype of over-expression in the non-host system, A. thaliana. I could demonstrate that Cab1 targets BIN2 (Shaggy-like kinase 3) at the C-terminal domain and re-localizes BIN2 from the cytosol to the nucleus. In the results of Cab1-Bin2 interaction in the non-host system, I showed 10 times more phosphorylation of AtBIN2 Tyrosine Y200, and five times less ubiquitination of AtBIN2-Lysine35 than the control. Respectively, these post-translation modifications correlate to higher activity and less degradation of AtBin2 in the presence of Cab1. The results of total RNA sequencing showed that Cab1 induction downregulates Samll Auxin Up-regulated RNAs (SAURs) and Expansins (EXPs)-mediated cell wall expansion which also aligns with our phenotypic observations and molecular studies. I showed the Cab1 mechanism to promote the AtBin2 active state in planta. The appendix contains my contributions to other unpublished studies in the lab during my Ph.D. career at Djamei lab.},
url = {https://hdl.handle.net/20.500.11811/11602}
}
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