Developmental profiles for two new embryo lethal mutants, dek22 and dek23

We have been studying the embryo development of two defective kernel mutants (cp*-E1113A and dcr*-E1428) previously reported (W.F. Sheridan and M.G. Neuffer, 1982) to lack leaf primordia at the mature kernel stage. These two mutants have been tested for allelism with the named dek mutants on 1L and 2L respectively, since the first mutant is on 1L (Sheridan and Neuffer 1981) and the second mutant is on 2L (Sheridan and Neuffer, in press). By use of a double pollination technique (MNL 58:92-95) we have demonstrated non-allelisin of cp*-E1113A with dek2 on 1L, and non-allelism of dcr*-E1428 with both dek4 and dek16 on 2L. Consequently we now designate cp*-E1113A as dek22 and dcr*-El428 as dek23.

Developmental profiles were obtained by examining mutant embryos at intervals from early in kernel development until maturity using paraffin sectioning, fresh dissection, and scanning electron microscopy techniques. Both dek22 and dek23 express their mutant phenotypes early in development. Mutant dek22 embryos reach the transition stage during early kernel development. They remain healthy and morphologically normal, but they are blocked in further growth and development. Mutant embryo expression is markedly uniform both with regard to size and stage of development. Mutant embryos of dek23 are variable in size but otherwise uniform in mutant phenotype. They reach an abnormal coleoptilar stage with a characteristic arrowhead shape during early kernel development and remain thereafter blocked at that stage, although they continue to enlarge. The mutant embryos fail to differentiate a shoot apex; instead, localized necrosis appears where a shoot apex would normally form, and subsequently spreads throughout the embryo. These two lethal mutants, blocked at different stages of embryo development, appear to define unique steps in the sequence of gene activities essential for normal embryogenesis. A detailed report on these two mutants will soon be submitted for publication in Developmental Biology.

William F. Sheridan and Janice K. Clark


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