Submitted to: Development
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 25, 2011
Publication Date: January 1, 2011
Citation: Yi, G., Moran Lauter, A., Scott, M.P., Becraft, P.W. 2011. The thick aleurone1 mutant defines a negative regulation of maize aleurone fate that functions downstream of dek1. Development. DOI: 10.1104/pp.111.177725. Interpretive Summary: Corn kernels are composed of different parts, each with specific biological roles. The process by which these different parts form is called development and is controlled by poorly understood genetic mechanisms. The objective of this work is to learn more about these genetic mechanisms. This manuscript reports characterization of a mutation called thick aleurone1 (thk1) that fails to develop normally. We examined thk1 by itself or in the presence of another mutation that also effects kernel development called defective kernel (dek1). Our results indicate that thk1 and dek1 function together to control development of the kernel. Understanding how different parts of a kernel develop may suggest strategies for improving grain quality or seed function. This will benefit the public by improving the quality and amount of corn grain, an important component of our food supply.
Technical Abstract: The maize aleurone layer occupies the single outermost layer of the endosperm. The dek1 gene is a central regulator required for aleurone cell fate specification. Dek1 mutants have pleiotropic phenotypes including lack of aleurone cells, aborted embryos, carotenoid deficiency and a soft, floury endosperm deficient in gamma zeins. Here we describe the thick aleurone1(thk1) mutant which defines a novel negative function in the regulation of aleurone differentiation. Mutants possess multiple layers of aleurone cells as well as aborted embryos. Clonal sectors of thk1 mutant tissue in otherwise normal endosperm showed localized expression of the phenotype with sharp boundaries indicating a localized cellular function for the gene. Sectors in leaves showed expanded epidermal cell morphology but the mutant epidermis generally remained in a single cell layer. Double mutant analysis indicated that the thk1 mutant is epistatic to dek1 for several aspects of the pleiotropic dek1 phenotype. Dek1 mutant endosperm that was mosaic for thk1 mutant sectors showed localized patches of thick aleurone. Localized sectors were surrounded by a halo of carotenoid pigments and double mutant kernels had restored zein profiles. In sum, loss of thk1 function restored the ability of dek1 mutant endosperm to accumulate carotenoids and zeins and to differentiate aleurone. Therefore the thk1 mutation defines a negative regulator that functions downstream of dek1 in the signaling system that controls aleurone specification and other aspects of endosperm development. The thk1 mutation was found to be caused by a deletion of approximately 2.3 megabases.