Analysis of four embryo-specific mutants in Zea mays reveals that incomplete radial organization of the proembryo interferes with subsequent development

Abstract

Using confocal laser scanning microscopy we have characterized early and intermediate stages of maize wild-type embryogenesis and compared to mutant development of four different embryo-specific mutations, emb *-8518, emb*-8521, emb*-8537, and emb*-8542. Confocal laser scanning microscopy is well suited to study embryo development in maize in a nondisruptive manner from shortly after fertilization to late stages in embryogenesis. The analysis of the mutant morphology indicated that two of the recessive mutations, emb*-8518 and emb*-8521, cause an early developmental arrest in the proembryo/early transition stage: mutant embryos are unable to enter the morphogenetic phase of embryogenesis. In contrast, homozygous emb*-8537, and emb*-8542 embryos progress at least to the coleoptilar stage and sometimes establish a functional shoot meristem that can determine leaf primordia. The morphological characterization of mutants was confirmed by analysis of the expression pattern of three different marker genes: Lipid transfer protein 2, Zea mays Outer Cell Layer 1, and Knotted 1. Our data indicate that both emb*-8518 and emb*-8521 mutant embryos are impaired in restriction of ZmOCL1 transcripts to the embryonic protoderm and therefore fail to establish a normal radial organization. In contrast, emb*-8537 and emb*-8542 embryos exhibit the wild-type pattern and proceed in development to the formation of a shoot apical meristem and the establishment of bilateral symmetry.

ZmPIN1-Mediated Auxin Transport Is Related to Cellular Differentiation during Maize Embryogenesis and Endosperm Development

“…As soon as polar localization of ZmPIN1 was observed in the apical anticlinal membranes of the embryo proper outer cell layer, differentiation of the protoderm started. It has been reported that the protoderm is the first evidence of differentiation in maize embryo (Elster et al, 2000), and we observed that this differentiation is correlated with high auxin accumulation.…”

“…At the end of the proembryo stage, the protoderm specifies as a single layer of homogenously sized peripheral cells surrounding the embryo proper. Maize mutants impaired in the restriction of embryonic protoderm-specific genes have been shown to fail in establishing a normal radial organization and to enter the morphological phase of embryogenesis (Elster et al, 2000). Embryonic differentiation continues with the adaxial/abaxial regionalization that is marked by the expression of ZmDRN (Zimmermann and Werr, 2005), a potential ortholog of the Arabidopsis DORNRÖ SCHEN (DRN), on the abaxial side, followed by lateral initiation of the shoot apical meristem (SAM) at the adaxial surface.…”

The maize duplicate genesnarrow sheath1andnarrow sheath2encode a conserved homeobox gene function in a lateral domain of shoot apical meristems

“…Still others suggest that the scutellum and coleoptile together comprise the apical and basal components of the single grass cotyledon, in which the scutellum represents the highly modified upper leaf component and the coleoptile represents the sheathing base of the cotyledon. Interesting maize mutants exist that lack a coleoptile, but show normal development of embryonic leaves (Elster et al, 2000). In addition, expression of the ltp2 (lipid transfer protein 2) gene is found in the outer cell layer of the scutellum and coleoptile, but is excluded from the L1 layer of the SAM and the epidermis of true leaf primordia (Sossountzov et al, 1991;Bommert and Werr, 2001).…”

PAHB1 is an evolutionary conserved HD‐GL2 homeobox gene expressed in the protoderm during Norway spruce embryo development

“…The drastic effects observed on embryo development using our transgenic approach is reminiscent of what has been described in two embryo-specific (emb) mutants emb*-8518 and emb*-8521 in maize (Elster et al, 2000). Unlike wild-type development, the expression of ZmOCL1, a cognate gene of PaHB1, is retained in the inner cells of the two mutant embryos.…”