Regulation of floral organ abscission in Arabidopsis thaliana

doi:10.1073/pnas.0805539105

Regulation of floral organ abscission in Arabidopsis thaliana

*Division of Biological Sciences, University of Missouri, Columbia, MO 65211;
^†Bond Life Sciences Center, University of Missouri, Columbia, MO 65211;
^‖Division of Biochemistry, University of Missouri, Columbia, MO 65211; and
^††Department of Life Science and Institute of Plant Biology, National Taiwan University, Taipei 10617, Taiwan

Edited by Joseph R. Ecker, The Salk Institute for Biological Studies, La Jolla, CA, and approved August 15, 2008 (received for review June 6, 2008)

Abstract

Abscission is a developmental program that results in the active shedding of infected or nonfunctional organs from a plant body. Here, we establish a signaling pathway that controls abscission in Arabidopsis thaliana from ligand, to receptors, to downstream effectors. Loss of function mutations in Inflorescence Deficient in Abscission (IDA), which encodes a predicted secreted small protein, the receptor-like protein kinases HAESA (HAE) and HAESA-like 2 (HSL2), the Mitogen-Activated Protein Kinase Kinase 4 (MKK4) and MKK5, and a dominant-negative form of Mitogen-Activated Protein Kinase 6 (MPK6) in a mpk3 mutant background all have abscission-defective phenotypes. Conversely, expression of constitutively active MKKs rescues the abscission-defective phenotype of hae hsl2 and ida plants. Additionally, in hae hsl2 and ida plants, MAP kinase activity is reduced in the receptacle, the part of the stem that holds the floral organs. Plants overexpressing IDA in a hae hsl2 background have abscission defects, indicating HAE and HSL2 are epistatic to IDA. Taken together, these results suggest that the sequential action of IDA, HAE and HSL2, and a MAP kinase cascade regulates the programmed separation of cells in the abscission zone.

Footnotes

^‡‡To whom correspondence may be addressed. E-mail: zhangsh{at}missouri.edu or walkerj{at}missouri.edu
Author contributions: S.Z. and J.C.W. designed research; S.K.C., C.T.L., D.C., H.W., and T.-L.J. performed research; S.K.C., C.T.L., D.C., H.W., and S.Z. contributed new reagents/analytic tools; S.K.C., C.T.L., D.C., H.W., T.-L.J., and S.Z. analyzed data; and J.C.W. wrote the paper.
↵^‡Present address: Delaware Biotechnology Institute, University of Delaware, Newark, DE 19711.
↵^§Present address: United States Department of Agriculture, Agriculture Research Service, Photosynthesis Research Unit and Department of Plant Biology, University of Illinois, Urbana, IL 61801.
↵^¶Present address: Department of Biological Sciences, Mississippi State University, Mississippi State, MS 39762.
↵**Present address: Monsanto, 700 Chesterfield Parkway West, Mail Zone GG4G, Chesterfield, MO 63017.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.