2017 ASHS Annual Conference
Investigating the Roles of the Plant Hormones Jasmonic Acid and Cytokinin in Control of Maize Leaf Growth
Investigating the Roles of the Plant Hormones Jasmonic Acid and Cytokinin in Control of Maize Leaf Growth
Friday, September 22, 2017: 3:15 PM
Kohala 3 (Hilton Waikoloa Village)
Plant growth is the accumulation of biomass due to both cell division and cell expansion. External challenges such as diseases and insect pests lead to reductions in growth and subsequent biomass loss. Thus, understanding the molecular basis of plant growth is important for agriculture and horticultural sciences and using a simple model to study growth is necessary to enable this type of research. In Zea mays (maize), growth is spatially separated into three distinct growth zones- division, elongation, and maturation- at the leaf base. This spatial separation makes the maize leaf a useful and simple model for investigating growth at the molecular and cellular levels. Our lab studies mutants that affect maize leaf growth as an entry into the molecular networks guiding growth. Using the semi-dominant maize mutant, Hairy Sheath Frayed (Hsf1), we showed that hypersignaling of the plant hormone cytokinin (CK) reduced leaf size. CK typically promotes cell division but can repress growth in certain tissues. Analysis of Hsf1 leaves indicated there was a decrease in the number of dividing cells and increased levels of the hormone jasmonic acid (JA) in the leaf growth zone. JA is known to reduce cell division in the model plant A. thaliana, implying that CK-signaling may restrict maize growth by influencing JA accumulation. To test this hypothesis, we determined (1) if exogenous JA could reduce maize leaf growth, (2) the effects of JA treatment on cell division and expansion, and (3) how responsive Hsf1 mutant plants were to JA treatment. Results from these tests showed that exogenous JA treatment dramatically reduced leaf growth primarily through reducing the length of time leaves grew. In addition, Hsf1 mutant plants had a limited response to JA treatment, indicating the JA response in this mutant background was already saturated. These data help explain the cause of growth reduction in Hsf1 and set the foundation for further molecular and histological studies to uncover the players that mediate this novel hormone interaction.