Abstract
Plastid gene expression is essential to embryogenesis in higher plants, but the underlying mechanism is obscure. Through molecular characterization of an embryo defective 16 (emb16) locus, here we report that the requirement of plastid translation for embryogenesis is dependent on the genetic background in maize (Zea mays). The emb16 mutation arrests embryogenesis at transition stage and allows the endosperm to develop largely normally. Molecular cloning reveals that Emb16 encodes WHIRLY1 (WHY1), a DNA/RNA binding protein that is required for genome stability and ribosome formation in plastids. Interestingly, the previous why1 mutant alleles (why1-1 and why1-2) do not affect embryogenesis, only conditions albino seedlings. The emb16 allele of why1 mutation is in the W22 genetic background. Crosses between emb16 and why1-1 heterozygotes resulted in both defective embryos and albino seedlings in the F1 progeny. Introgression of the emb16 allele from W22 into A188, B73, Mo17, Oh51a and the why1-1 genetic backgrounds yielded both defective embryos and albino seedlings. Similar results were obtained with two other emb mutants (emb12 and emb14) that are impaired in plastid protein translation process. These results indicate that the requirement of plastid translation for embryogenesis is dependent on genetic backgrounds, implying a mechanism of embryo lethality suppression in maize.
Highlights
Embryogenesis in flowering plants initiates with fertilization of one sperm cell with the egg, and ends with the formation of a basic plant body including shoot and root meristems
Further genetic analyses demonstrate that the requirement of WHY1 function for embryogenesis is dependent on the genetic background. This dependence exists in two other embryo defective genes that affect plastid translation. These results indicate that the requirement of plastid translation for embryogenesis may not be related with the expression of maize plastid genome, and it should be independent of the fatty acid synthesis pathway [6]
We revealed that the arrest of embryogenesis in the maize emb16 mutant is caused by a mutation in Why1 gene, demonstrating that embryogenesis requires the function of Why1
Summary
Embryogenesis in flowering plants initiates with fertilization of one sperm cell with the egg, and ends with the formation of a basic plant body including shoot and root meristems. This process requires the functions of many genes. The embryogenic mutants are classified into defective kernel, empty pericarp, small kernel and embryo defective (emb) based on the impact on the embryo and endosperm. The emb subclass in maize describes seed mutants with specific arrest in embryo development and without significant deleterious impact on endosperm development [5]
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