Developmental profiles of three embryo‐lethal maize mutants lacking leaf primordia:ptd*‐1130,cp*‐1418, andbno*‐747B
作者:
William F. Sheridan,
Yvonne R. Thorstenson,
期刊:
Developmental Genetics
(WILEY Available online 1986)
卷期:
Volume 7,
issue 1
页码: 35-49
ISSN:0192-253X
年代: 1986
DOI:10.1002/dvg.1020070104
出版商: Wiley Subscription Services, Inc., A Wiley Company
关键词: zea mays;embryogenesis;defective kernel mutants;genetic regulation;maize;leaf primordia
数据来源: WILEY
摘要:
AbstractThe defective kernel (dek) mutants of maize are altered in both their embryo and endosperm development. Earlier studies have indicated that some of thedekmutants are unable to form shoot apical meristems or leaf primoirda. We have examined three embryo lethaldekmutants of this type,ptd*‐1130,cp*‐1418, andbno*‐747B, to obtain a developmental profile for each. Allelism tests show that these three mutants are not allelic. Embryos were examined in early, mid‐, and late kernel development as well as at kernel maturity by dissection and sectioning procedures and also at kernel maturity by scanning electron microscopy. All three mutants lag behind normal embryos in their rate of development. Embryos ofptd*‐1130reached the transition stage by early kernel development and progressed no further but underwent cell enlargement and necrosis during late kernel development. Embryos ofcp*‐1418reached an early coleoptilar stage by midkernel development. They subsequently increased in size but did not form any leaf primordia. At kernel maturity, they no longer had a shoot apical meristem but often had a well formed root meristem. They appeared to remain healthy and did not become necrotic. Embryos ofbno*747Breached the early coleoptilar stage by early kernel development but progressed no further. By kernel maturity, they had grown into masses of irregularly shaped embryonic tissue that no longer resembled any normal embryo stage but were not necrotic. None of these three mutants responded to attempts to support continued embryo development when cultured, but all three mutants formed callus on N6 and MS media supplemented with 2,4‐D. These results indicate that these mutants are all uniformly blocked at specific stages early in embryonic development, have different subsequent developmental fates, and represent three different genes performing unique functions that are essential for
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