Description
TitleRegulation of cell polarity in stomatal asymmetric cell division in Arabidopsis
Date Created2017
Other Date2017-10 (degree)
Extent1 online resource (xii, 118 p. : ill.)
DescriptionCell polarization, manifested by the asymmetric distribution of intracellular molecules, structures and functions within a cell, is an essential feature and plays critical roles in development and environmental responses for almost all cellular organisms. Polarly localized proteins at the cell cortex are key to asymmetric cell division (ACD), a fundamental process underlying the precise control of self-renewal and differentiation of stem cells in both animals and plants. The BREAKING OF ASYMMETRY IN THE STOMATAL LINEAGE (BASL) protein was one of the first polarity factors identified to control stomatal ACD in Arabidopsis. Remarkably, the localization and function of this plant-specific polarity protein resemble that of the conserved PAR protein complexes in animal ACD. However, how BASL protein is polarized to the cell cortex and how its polarity is precisely maintained at the plasma membrane have been major questions in the field. My Ph.D. research aimed to address these fundament questions. Presented in this dissertation are my genetic, molecular and cell biological data that implicate novel mechanisms for polarity establishment, maintenance, and attenuation in the stomatal lineage cells. Chapter 2 describes a positive genetic interaction between BASL and the MAPKK kinase YODA (YDA). My collaboration effort with Dr. Ying Zhang (the Dong Lab) and Dr. Pengcheng Wang (the Zhu Lab at Purdue U.) demonstrated that a canonical MAPK signaling pathway is integrated into the BASL polarization process during stomatal ACD (Zhang et al., 2015). My results show that YDA physically interacts and co-polarizes with BASL in the stomatal ACD cells, providing a molecular basis for the forward feedback loop between BASL and the MAPK signaling pathway in the establishment of cell polarity. The identification of this positive feedback loop and the differential expression of the polarity complex in two daughter cells also provided new insights into the mechanism for differential daughter cell fate determination in plants (Zhang et al., 2016b). To understand how this self-amplifying, positive feedback signaling system is maintained and attenuated in plant cells, I characterize the subcellular distribution and dynamic trafficking of BASL and YDA (Chapter 3). My cell biological data demonstrated that the PM-associated BASL and YDA proteins are internalized into the endomembrane system and delivered to MVB and vacuole for degradation in the stomatal lineage cells. It is therefore hypothesized that the plasma membrane-associated BASL and YDA proteins are subjected to an elegant regulation by endomembrane trafficking so that the amount of active molecules and the distribution pattern can be dynamically and precisely controlled in cell development. In Chapter 4, I studied a newly identified polarity regulator ICR1. I found that ICR1 promotes the vacuolar degradation of internalized BASL and YDA, thus alleviates the positive feedback signaling at the plasma membrane. More interestingly, ICR1 is a plant-specific, MT-binding protein, thus revealing a new role of MT cytoskeleton in the regulation of vacuolar trafficking in plant cells. In addition, my collaboration with Dongmeng Li (the graduate student in the Dong Lab) links the function of ICR1 with FAB1/PIKfyve (Phosphatidylinositol 3-phosphate 5-kinase), an important player in promoting endosome maturation, in vacuolar targeting and degradation of BASL-YDA. Overall, my work contributes to the formulation of the BASL-centered polarization machinery that was promoted by a positive feedback regulation with a MAPK signaling pathway and downregulated by a MT-based ICR1 vacuolar targeting system to achieve dynamic and precise spatiotemporal control on subsequent developmental processes.
NotePh.D.
NoteIncludes bibliographical references
Noteby Wanchen Shao
Genretheses, ETD doctoral
Languageeng
CollectionSchool of Graduate Studies Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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