Cell 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.
Subject (authority = RUETD)
Topic
Plant Biology
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_8342
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (xii, 118 p. : ill.)
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Subject (authority = ETD-LCSH)
Topic
Polarity (Biology)
Subject (authority = ETD-LCSH)
Topic
Cell differentiation
Note (type = statement of responsibility)
by Wanchen Shao
RelatedItem (type = host)
TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.