Control of Arabidopsis vein-network formation by cell proliferation

• Author / Creator

  Odat, Osama

• In most multicellular organisms, signals and nutrients are transported throughout the body by a vascular system. For normal development and optimal function, no area of the body should thus be devoid of vessels. Therefore, the growth of tissues and their vascularization must be tightly coordinated, and understanding the molecular basis of this coordination is a key question in biology. In animals, signals from proliferating nonvascular tissues promote their vascularization; in turn, vessels signal back to surrounding nonvascular tissues to control their growth and development. By contrast, in plant organs, vascular and nonvascular tissues differentiate from the same precursor cells; yet it is possible that the logic that integrates the growth of tissues and their vascularization in plants is no different from that in animals. Here, I investigated this possibility for Arabidopsis leaves, in which internal, ground cells proliferate and differentiate into either mesophyll or veins. I combined: (i) molecular genetic interference with core regulators of cell cycle progression and cell differentiation; (ii) cellular imaging of cell fate markers; and (iii) analysis of vein network topology. And I used this combined approach to show that cell proliferation inhibits progression of ground cells to mesophyll fate, thus permitting their recruitment into veins, and that cessation of cell proliferation permits progression of ground cells to mesophyll fate, thus preventing their recruitment into veins. Though this logic resembles that of tissue patterning in animal appendages, it is different from that which integrates tissue growth and vascularization in animal organs. What molecular mechanisms control the integration of tissue growth and vascularization in plant organs? By combining (i) molecular genetic interference with core regulators of cell cycle progression and signaling pathways, (ii) topological analysis of vein networks, and (iii) imaging of cell proliferation markers, I show that leaf growth and vascularization are integrated by the activity of two pathways that antagonistically control cell proliferation and vein network formation: transcriptional input provided by the CINCINNATA-related TCP (for TEOSINTE BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTOR) proteins inhibits these processes; transduction of the signaling molecule auxin mediated by the MONOPTEROS transcription factor promotes them. My results thus suggest a molecular mechanism that controls the unique logic by which timing of cessation of cell proliferation integrates tissue growth and vascularization in plants.

• Subjects / Keywords

  • Arabidopsis
  • Vascular
  • Proliferation

• Graduation date

  Fall 2015

• Type of Item

  Thesis

• Degree

  Doctor of Philosophy

• DOI

  https://doi.org/10.7939/R38W38975

• License

  This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.