Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 2/25/2011
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: The Mn1 locus is a major determinant of sink strength of developing seeds through its control of both sink size, i.e., cell size and cell number, and sink activity via sucrose hydrolysis and the release of hexoses essential for energy and signaling functions. Hexoses are also essential for the development of basal endosperm transfer cells (BETCs), the sole gateway for sugars and other nutrients from the pedicel. Not surprisingly, loss-of-function mutations at the Mn1 locus lead to the mn1 seed phenotype that show ~ 70% reduction in seed mass at maturity and several pleiotropic changes, including the altered levels of auxin, IAA, and cytokinins in the developing endosperm. Previously we reported an EMS-induced semi-dominant allele, mn1-89, showing higher levels of the Mn1 RNA but greatly reduced CWI activity (~6% of the WT); however, the seed phenotype is near-normal. We show here that seed mass in the mn1-89, its reciprocal hybrids with mn1-1, and the mn1-1 (a null allele) was dependent on the number of mn1-89 alleles in the endosperm. The Mn1 RNA levels were also gene-does dependent by q-PCR analyses; a similar correlation with the CWI activity is shown previously (Plant Cell 8: 971). However, no such correlation was seen in the levels of IAA and a major cytokinin, zeatin, in 12 DAP endosperm. A comparative analysis of endosperm and embryo mass in the Mn1 and mn1-1 at 12, 20 and 28 DAPs showed significant reductions of both tissues in the mn1-1 for all three stages. Clearly, embryo development was endosperm-dependent. To gain a mechanistic understanding of this interaction, sugar levels were measured in these samples. Levels of all three major sugars, glc, fru and suc, in the embryos reflected a pattern similar to its endosperm, indicating a metabolic-dependence or -cross-talk between endosperm and embryo despite the well documented evidence of their genetic autonomy in sugar / starch pathways.