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The maize gene empty pericarp‐2 is required for progression beyond early stages of embryogenesis
Author(s) -
Scanlon Michael J.,
Myers Alan M.,
Schneeberger Richard G.,
Freeling Michael
Publication year - 1997
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.1997.12040901.x
Subject(s) - biology , meristem , scutellum , endosperm , coleoptile , mutant , embryo , embryogenesis , genetics , mutation , suspensor , microbiology and biotechnology , gene , botany , zygote
Summary The defective kernel mutation empty pericarp2‐R ( emp2‐R ) causes retardation and subsequent abortion of maize kernel development. Analyses of genetic aneuploid kernels indicate that the embryo phenotype is not dependent on the endosperm genotype; the mutation conditions embryo defects even in the presence of a normal endosperm. Embryos reach an abnormal coleoptilar stage before aborting and disintegrating. The mutants form primary embryonic organs only; the scutellum and coleoptile develop, but no leaves are formed. Immunohisto‐localization studies utilized KNOX homeodomain proteins as markers of meristem formation and identity. These analyses indicate that the shoot meristem forms in emp2‐R mutant embryos, but does not mature to a tunica‐corpus shape. No evidence of leaf founder cell initialization was revealed in the mutant meristems. These data indicate that the emp2 gene may be required for embryogenic patterning beyond the coleoptilar stage of development.