Purdue News

October 31, 2005

Newly recognized gene mutation may reduce seeds, resurrect plants

WEST LAFAYETTE, Ind. – A mutated plant that seems to return from the dead may hold the secret to how some flora protect their progeny during yield-limiting drought and other stresses, according to Purdue University scientists whose study of the plant led to discovery of a gene.

Matt Jenks

The gene, called RESURRECTION1 (RST1), has revealed a previously unknown genetic connection between lipid development and embryo development in plants, said Matthew Jenks, lead author of the study and a Purdue plant physiologist.

Lipids play a role in preventing plant dehydration in forming cells' membranes, in molecular signaling and in energy storage. A still-to-be revealed lipid associated with formation of the cuticle that coats plant surfaces may signal whether a seed develops to maturity or is aborted early due to a defective embryo.

"This is interesting because in crop production a number of plants have a problem of reduced yield due to seed or fruit abortion," Jenks said. "It's thought that plants may abort some of their seeds, especially under stress, to conserve and divert resources to the remaining seeds. So, in a drought situation, for example, plants will get rid of some seeds so that they can support growth of at least a few healthy seeds."

In the November issue of Plant Physiology, Jenks and his team of researchers from the Purdue Department of Horticulture and Landscape Architecture report on the normal gene RST1.

They found the gene while studying a unique surface wax mutant of Arabidopsis, a common laboratory research plant. All plants have a certain amount of wax overlaying leaves and stems.

The abnormal plant, a mutant of RST1, had short, rounded leaves that turned purple during development, and then before flowering, the plant quickly browned and looked dead. It also had a large proportion of small, wrinkled, non-viable seeds with aborted embryos. These contained only 34 percent of the normal amount of lipids.

"It appeared to have died, and I left it in a room for two or three weeks. I was just slow in throwing it away," said Jenks, who also is a member of the Purdue Center for Plant Environmental Stress Physiology. "When I went to throw it away, I noticed it had small shoots coming up as if it had returned to life."

The surprising finding in studying the mutant was that a single gene could affect so many diverse traits, Jenks said. Another somewhat similar mutant Arabidopsis showed alterations only in wax and seed development, but not in the other mutated RST1 traits. This was a major clue that changes in lipid synthesis were somehow altering seed development.

Scientists already know that lipids play an important role in signaling developmental changes in plants and animals, and that other plants and animals, including humans, have genes similar to RST1. Jenks and his team now want to determine the exact role of RST1 in lipid signaling that affects plant development, particularly its role in crop seed self-thinning mechanisms through embryo abortion.

Unlike some other mutants that abort all of its seeds, the mutant RST1 plant aborts only about 70 percent of the seeds, he said.

"RST1 is not required for seed development, but it does influence how seeds develop, perhaps playing a role in regulating the number of seeds a plant will support to maturity," Jenks said. "Seed abortion by plants likely is a tightly regulated process that necessitates allowing some seed loss to conserve resources in a stressful environment without aborting all seeds, which would leave the plant with no healthy offspring."

If researchers learn how to control plant embryo abortion, they may be able to increase yield by helping plants shed fewer seeds, grains or fruits, especially under drought conditions and in other stressful environments.

U.S. Department of Agriculture National Research Initiative and the SALK Institute Genomic Analysis Laboratory provided support for this work.

The other researchers involved in the study were Ray Bressan, Purdue Department of Horticulture and Landscape Architecture professor; Xinbo Chen, Xionglun Liu and Xinlu Chen, all horticulture postdoctoral students; and S. Mark Goodwin, a horticulture doctoral student.

Writer: Susan A. Steeves, (765) 496-7481, ssteeves@purdue.edu

Source: Matthew Jenks, (765) 494-1332, jenksm@purdue.edu

Ag Communications: (765) 494-2722; Beth Forbes, forbes@purdue.edu
Agriculture News Page

Note to Journalists: The paper is currently published in the online version of Plant Physiology and scheduled for the journal's November issue.


A mutant Arabidopsis that seemed to rise from the dead helped Purdue plant physiologist Matthew Jenks and his research team find a genetic connection between lipid synthesis and embryo development in plants. The abnormal plant helped them discover a new gene they dubbed Resurrection that apparently plays a part in lipid signaling of seed abortion. (Purdue Agricultural Communications photo/Tom Campbell)

A publication-quality photo is available at https://news.uns.purdue.edu/images/+2005/jenks-resurrection.jpg




Mutation of the RESURRECTION1 Locus of Arabidopsis Reveals an Association of Cuticular Wax with Embryo Development

Xinbo Chen, S. Mark Goodwin, Xionglun Liu, Xinlu Chen, Ray A. Bressan, Matthew A. Jenks *

Crop Gene Engineering Key Laboratory of Hunan Province, Hunan Agricultural University, Changsha, China, 410128

Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, Indiana 47907 – * Corresponding author; email: jenksm@purdue.edu

Insertional mutagenesis of Arabidopsis (Arabidopsis thaliana) was used to identify a novel recessive mutant, designated resurrection1 (rst1), which possesses a dramatic alteration in its cuticular waxes and produces shrunken nonviable seeds due to arrested embryo development. The RST1 gene sequence associated with these phenotypes was verified by three independent, allelic, insertion mutants, designated rst1-1, rst1-2, and rst1-3, with inserts in the first exon, 12th intron, and fourth exon, respectively. These three rst1 allelic mutants have nearly identical alterations in their wax profiles and embryo development. Compared to wild type, the wax on rst1 inflorescence stems is reduced nearly 60% in total amount, has a proportional reduction in aldehydes and aldehyde metabolites, and has a proportional increase in acids, primary alcohols and esters. Compared to wild type, the C29 alkanes on rst1 are nearly sixfold lower, and the C30 primary alcohols are fourfold higher. These results indicate that rst1 causes shunting of most wax precursors away from alkane synthesis and into the primary alcohol-producing branch of the pathway. In contrast to stems, the wax on rst1 mutant leaves increased roughly 43% in amount relative to the wild type, with the major increase occurring in the C31 and C33 alkanes. Unique among known wax mutants, approximately 70% of rst1 seeds are shrunken and nonviable, with these being randomly distributed within both inflorescence and silique. Viable seeds of rst1 are slightly larger than those of wild type, and although the viable rst1 seeds contain more total triacylglycerol-derived fatty acids, the proportions of these fatty acids are not significantly different from wild type. Shrunken seeds contain 34% of the fatty acids of wild-type seeds, with proportionally more palmitic, stearic and oleic acids, and less of the longer and more desaturated homologs. Histological analysis of aborted rst1 seeds revealed that embryo development terminates at the approximate heart-shaped stage, whereas viable rst1 and wild-type embryos develop similarly. The RST1 gene encodes a predicted 1,841-amino acid novel protein with a molecular mass of 203.6 kD and a theoretical pI of 6.21. The RST1 transcript was found in all tissues examined including leaves, flowers, roots, stems and siliques, but accumulation levels were not correlated with the degree to which different organs appeared affected by the mutation. The new RST1 gene reveals a novel genetic connection between lipid synthesis and embryo development; however, RST1's exact role is still quite unknown. The degree to which RST1 is associated with lipid signaling in development is an important focus of ongoing studies.


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