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ARS Home » Southeast Area » Gainesville, Florida » Center for Medical, Agricultural and Veterinary Entomology » Chemistry Research » Research » Publications at this Location » Publication #339995
Title: Investigating the roles of jasmonic acid and cytokinin in maize leaf growth control

Author
item UYEHARA, AIMEE - University Of Hawaii
item CAHILL, JAMES - University Of Hawaii
item Hunter, Charles
item MUSZYNSKI, MICHAEL - University Of Hawaii

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/12/2017
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Plant growth is the accumulation of biomass attributed to cell division and cell expansion. In the maize leaf, growth is spatially separated into three distinct growth zones: the division zone, elongation zone, and the maturation zone. This spatial separation makes the maize leaf a useful model for understanding growth because changes in the cellular morphology of these growth zones reflects changes in the underlying molecular networks driving growth. We previously showed that the semi-dominant maize mutant, Hairy Sheath Frayed (Hsf1) was caused by hypersignaling of the plant hormone cytokinin (CK) which 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 which was associated with increased levels of jasmonic acid (JA), a defense and growth repressive hormone. JA is known to reduce cell division in A. thaliana implying that CK-signaling may restrict maize growth through upregulating the JA pathway. To test this idea, we adapted our maize seed hormone assay to establish the effects of exogenous JA application on maize leaf growth. B73 seeds treated with JA exhibited a significant reduction in leaf size and a decreased leaf elongation rate. Next, JA treatments were done on Hsf1/+ and WT-sib seedlings. JA treatments resulted in a greater reduction in leaf size in WT-sibs compared to JA-treated Hsf1/+, suggesting that JA perception is already saturated in Hsf1 mutants. Treatments are being repeated to confirm these results. These data help explain the cause of growth reduction in Hsf1 and set the foundation for further molecular and histological tests of JA-mediated growth changes downstream of CK signaling.