Morphological studies on five embryo-lethal mutants

Five embryo-lethal mutants of maize were examined from early in kernel development when they first became distinguishable through later stages until maturity using North Dakota grown material. Mutant and normal kernels were fixed and examined by histological techniques. Three of the mutants (E747B, E1130, E1418) did not form leaf primordia during embryo development while one (E1425A) did so rarely. The fifth mutant, E1311C, formed several leaf primordia by kernel maturity but was unable to germinate when cultured or when mature mutant kernels were planted.

All of the mutants were blocked at a specific stage in embryonic development, except E1425A which was variable. The mutant E747B developed normally to the coleoptilar stage, forming a shoot apical meristem and an embryonic axis. The embryo subsequently underwent unorganized proliferation and necrosis. By kernel maturity, no organized structures were apparent.

Embryogenesis in the mutant E1130 began with the formation of a fairly normal transition stage embryo. However, the mutant embryos did not proceed to form either shoot or root apical meristems. At maturity, the embryos still retained a transition stage shape, but were larger than normal with vacuolated cells, and a wrinkled appearance.

The embryos of E1418 began their development normally. However, after the transition stage, they elongated and formed a root apical meristem and in some cases a rudimentary shoot apical meristem. Then the shoot apical meristem stopped developing while the root apical meristem continued development. In one mature mutant embryo, a necrotic area on the face of the embryo marked where the shoot apical meristem would normally be located.

Embryos of E1425A were variable in their development. In some cases, the embryos were small, necrotic and malformed. In other cases, they appeared to be more normal, even to the extent of leaf primordia formation in one case. The variability was seen in kernels from the same ear as well as between ears. One possible explanation for this phenomenon is the existence of a modifier gene for the expression of E1425A.

The last mutant, E1311C, was normal throughout embryogenesis except that its development was slowed and it was smaller at maturity. In addition, the mature embryo axis was bent at an abnormal angle, resulting in the misalignment of the shoot and root apical meristems.

Yvonne R. Potts and William F. Sheridan

Please Note: Notes submitted to the Maize Genetics Cooperation Newsletter may be cited only with consent of the authors.

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