Embryo developmental profiles of cp*-1379A, dscptd*-1425A, and dek17: three embryo-lethal mutants --Guy E. Farish and William F. Sheridan The three embryo-lethal defective kernel (dek) mutations are defective in both their endosperm and embryo development. Standard histological and fresh dissection techniques were used to examine and compare mutant and normal kernels from the same ears at ages ranging from 5-6 days after pollination (dap) through kernel maturity. Embryo stages are those of E. C. Abbe and O. L. Stein (Amer. J. Bot. 41:285-293, 1954). Two of the mutants are affected early in embryo morphogenesis while the third, dek17 on chromosome arm 3L, is capable of forming one or more leaf primordia but is unable to germinate.

The mutant cp*-1379A, also on 3L but not allelic to dek17, is blocked early in embryogenesis. By 12 dap, mutant embryos were lagging behind normal embryos on the same ear. Normal embryos were at a late transition stage while mutant embryos had not progressed beyond an early proembryo stage. At 18 dap mutant embryos reached a mid-transition stage and did not proceed beyond this with regard to formation of a coleoptilar ring or a shoot apical meristem, morphological features characteristic of the coleoptilar stage. Mutant embryos did become broadened so as to become uniformly shell-like in appearance. Because the mutant embryos lacked shoot meristems and leaf primordia they were unable to germinate at maturity.

The mutant dscptd*-1425A, located on chromosome arm 6L, is also disturbed early in embryogenesis. Mutant embryos lagged behind normal embryos in their development by 18 dap when normal embryos were at stage 1 while mutant embryos were at a mid-transition stage. By 32 dap normal embryos were at stage 4 while the mutant embryos varied in their progression so that they ranged from a late transition to an abnormal coleoptilar stage. None of the mutant embryos ever formed leaf primordia by kernel maturity and all were abnormal in appearance. Because the mutant embryos lacked leaf primordia they were unable to germinate at maturity.

Mutant dek17 embryos could not be distinguished from normal embryos until 18 dap. At this age, mutant embryos were at an abnormal late transition stage and normal embryos were at the coleoptilar stage. Mutant embryos continued to develop at a much slower rate than normal embryos; at 45 dap mutant embryos had formed a shoot apical meristem, a root meristem, a coleoptile, and one leaf primordium whereas normal embryos were at stage 5 (5 leaf primordia formed). Despite the presence of at least one leaf primordium, mutant embryos were unable to germinate at kernel maturity. The pleiotropism of this mutation results in a collapsed endosperm, a much delayed but otherwise essentially normal embryo morphogenesis, and a blockage to the escape of the embryo from dormancy.

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