Date of Award

December 2017

Document Type


Degree Name

Doctor of Philosophy (PhD)


Genetics and Biochemistry

Committee Member

Hong Luo

Committee Member

Julia Frugoli

Committee Member

Rajandeep Sekhon

Committee Member

Liangjiang Wang


The spectacular array of diverse plant forms as well as the predominantly sessile life style of plants raises two questions that have been fascinating to scientists in the field of plant biology for many years: 1) how do plants develop to a specific size and shape? 2) how do plants respond to environmental stresses given its immobility?

Plant organ development to a specific size and shape is controlled by cell proliferation and cell expansion. While the cell proliferation process is extensively studied, the cell expansion process remains largely unknown, and can be affected by several factors, such as cell wall remodeling and the incorporation of new wall materials. To better understand the genetic basis of plant development, we identified an Arabidopsis T-DNA insertion mutant named development related Myb-like 1 (drmy1), which showed altered size and shape in both vegetative and reproductive organs due to defective cell expansion. We further demonstrated that the defective cell expansion in the drmy1 mutant is linked to the change in cell wall composition. Complementation testing by introduction of DRMY1 into the mutant background rescued the phenotype, indicating that DRMY1 is a functional regulator of plant organ development. The DRMY1 protein contains a single Myb-like DNA binding domain and is localized in the nucleus, and may cooperate with other transcription factors to regulate downstream gene expression as DRMY1 itself does not possess transactivation ability. DRMY1 expression analysis revealed that its expression is reduced by the plant hormone ethylene (a negative regulator of cell expansion) while induced by ABA (a positive regulator of cell expansion). Furthermore, whole transcriptome profiling suggested that DRMY1 might control cell expansion directly by regulating genes related to cell wall biosynthesis/remodeling and ribosome biogenesis or indirectly through regulating genes involved in ethylene and ABA signaling pathways.

Plants cannot “escape” from salinity stress but have evolved different mechanisms for salt tolerance over the time of adaptation to salinity. About 1% of plant species named halophytes can survive and thrive in environments containing high salt concentrations, which makes it important to understand their salt tolerance mechanisms and the responsible genes. Here, we investigated salt tolerance mechanisms in Supreme, the most salt-tolerant cultivar of a halophytic warm-seasoned perennial grass, Seashore paspalum (Paspalum vaginatum) at the physiological and transcriptomic levels by comparative study with another cultivar Parish, which possesses moderate salinity tolerance. Our results suggest that Na+ accumulation under normal conditions and further increased accumulation under high salinity conditions (400 mM NaCl), possibly by vacuolar sequestration is a crucial mechanism for salinity tolerance in Supreme. Our data suggests that Na+ accumulation in Supreme under normal conditions might trigger the secondary messenger Ca2+ for signal transduction and the resulting upregulation of salt stress related transcription factors in addition to serving as cheap osmolytes to facilitate water uptake. Moreover, the retention of K+ under salt treatment, which can counteract the toxicity of Na+, is a protective mechanism for both cultivars. A strong oxidation-reduction process and nucleic acid binding activity under high salinity conditions are two other contributors to the salinity tolerance in both cultivars. We also identified ion transporters including NHXs and H+-PPases for Na+ sequestration and K+ uptake transporters, which can be used as candidate genes for functional studies and potential targets to engineer plants for enhanced salinity tolerance, opening new avenues for future research.



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