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pubmed:abstractText |
The heat shock response (HSR) is an evolutionarily conserved molecular/biochemical reaction to thermal stress that is essential to the survival of eukaryotic organisms. Recessive Mutator transposon mutations at the maize empty pericarp2 (emp2) locus led to dramatically increased expression of heat shock genes, retarded embryo development, and early-stage abortion of embryogenesis. The developmental timing of emp2 mutant embryo lethality was correlated with the initial competence of maize kernels to invoke the HSR. Cloning and sequence analyses revealed that the emp2 gene encoded a predicted protein with high similarity to HEAT SHOCK BINDING PROTEIN1, which was first described in animals as a negative regulator of the HSR. emp2 is a loss-of-function mutation of an HSR-negative regulator in plants. Despite the recessive emp2 phenotype, steady state levels of emp2 transcripts were abundant in mutant kernels, and the predicted coding region was unaffected. These expression data suggest that emp2 transcription is feedback regulated, whereas S1 nuclease mapping suggests that emp2 mutant transcripts are 5' truncated and nontranslatable. In support of this model, immunoblot assays revealed that EMP2 protein did not accumulate in mutant kernels. These data support a model whereby an unattenuated HSR results in the early abortion of emp2 mutant embryos. Furthermore, the developmental retardation of emp2 mutant kernels before the HSR suggests an additional role for EMP2 during embryo development distinct from the HSR.
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