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Carly
Shanks
Author
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling.
In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
Spring 2017
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling
in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth
and development, including cell division, meristem maintenance, sink/source relationships,
nutrient up-take, vascular development, and biotic and abiotic stress responses. The
cytokinin signal is relayed through a two-component signaling system and ultimately leads
to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are
transcriptionally up-regulated in response to cytokinin and are stabilized by
phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative
regulators of cytokinin signaling and participate in a negative feedback loop to reduce
cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact
with other target proteins to negatively regulate the pathway, however, the mechanism has
remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In
this study, the type-A ARRs are implicated in multiple plant processes, including nematode
infection, transcription factor regulation, and interaction with the exocyst complex. For
example, we find defense response genes are basally up-regulated in the type-A
arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are
hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR
function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found
that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6)
transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research
suggests that the BPC proteins are part of a network of transcription factors that
regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to
modify their activity. Furthermore, we find that the Exo70D proteins are positive
regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate
type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple
roles of the type-A ARRs and how they regulate cytokinin responsiveness.
Spring 2017
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting
institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
Spring 2017
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017-05
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph J.
Kieber
Thesis advisor
Joseph J.
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shank
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
Biology
Joseph J.
Kieber
Thesis advisor
Joseph J.
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shank
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
University of North Carolina at Chapel Hill
Degree granting institution
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph
Kieber
Thesis advisor
Joseph
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shanks
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
Biology
Joseph J.
Kieber
Thesis advisor
Joseph J.
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shank
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
University of North Carolina at Chapel Hill
Degree granting institution
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Biology
Joseph J.
Kieber
Thesis advisor
Joseph J.
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shank
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Carly
Shanks
Creator
Department of Biology
College of Arts and Sciences
The mechanism of type-A Arabidopsis response regulators in cytokinin signaling in Arabidopsis thaliana
Cytokinin is a phytohormone that regulates numerous processes in plant growth and development, including cell division, meristem maintenance, sink/source relationships, nutrient up-take, vascular development, and biotic and abiotic stress responses. The cytokinin signal is relayed through a two-component signaling system and ultimately leads to changes in gene expression. The type-A Arabidopsis response regulators (ARRs) are transcriptionally up-regulated in response to cytokinin and are stabilized by phosphorylation of their receiver domain. The ten type-A ARRs act as redundant negative regulators of cytokinin signaling and participate in a negative feedback loop to reduce cytokinin responsiveness. Previous studies have suggested that the type-A ARRs interact with other target proteins to negatively regulate the pathway, however, the mechanism has remained unclear. Here we explore how the type-A ARRs regulate cytokinin signaling. In this study, the type-A ARRs are implicated in multiple plant processes, including nematode infection, transcription factor regulation, and interaction with the exocyst complex. For example, we find defense response genes are basally up-regulated in the type-A arr3,4,5,6,7,8,9,15 loss-of-function mutant, and upon nematode infection these genes are hyper-induced, which leads to decreased pathogen success. To further examine type-A ARR function, we conducted a yeast two-hybrid screen for type-A ARR binding partners and found that the type-A ARRs interact with a member of the BASIC PENTACYSTEINE (BPC6) transcription factor family and a subunit of the exocyst complex, Exo70D3. Our research suggests that the BPC proteins are part of a network of transcription factors that regulates cytokinin response genes, and the type-A ARRs interact with BPC proteins to modify their activity. Furthermore, we find that the Exo70D proteins are positive regulators of cytokinin signaling and our data suggest that the Exo70D proteins regulate type-A ARR protein levels. Overall, we provide some mechanistic insight into the multiple roles of the type-A ARRs and how they regulate cytokinin responsiveness.
2017
Biology
Molecular biology
Cellular biology
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Joseph J.
Kieber
Thesis advisor
Joseph J.
Kieber
Thesis advisor
Jason
Reed
Thesis advisor
Elizabeth
Shank
Thesis advisor
Daniel
McKay
Thesis advisor
Zachary
Nimchuk
Thesis advisor
text
2017-05
Shanks_unc_0153D_16953.pdf
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2019-07-06T00:00:00
proquest
2017-04-23T14:11:18Z
yes
application/pdf
26252802