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Plant J. 2014 Jul;79(2):192-205. doi: 10.1111/tpj.12568. Epub 2014 Jun 23.

A pair of homoeolog ClpP5 genes underlies a virescent yellow-like mutant and its modifier in maize.

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1
National Maize Improvement Center, China Agricultural University, 2 West Yuanmingyuan Rd., Beijing, 100094, China; DuPont Pioneer, 200 Powder Mill Road, Wilmington, DE, 19880, USA.

Abstract

Gene-background interaction is a commonly observed phenomenon in many species, but the molecular mechanisms of such an interaction is less well understood. Here we report the cloning of a maize mutant gene and its modifier. A recessive mutant with a virescent yellow-like (vyl) phenotype was identified in an ethyl methanesulfonate-mutagenized population derived from the maize inbred line B73. Homozygous mutant maize plants exhibited a yellow leaf phenotype after emergence but gradually recovered and became indistinguishable from wild-type plants after approximately 2 weeks. Taking the positional cloning approach, the Chr.9_ClpP5 gene, one of the proteolytic subunits of the chloroplast Clp protease complex, was identified and validated as the candidate gene for vyl. When introgressed by backcross into the maize inbred line PH09B, the mutant phenotype of vyl lasted much longer in the greenhouse and was lethal in the field, implying the presence of a modifier(s) for vyl. A major modifier locus was identified on chromosome 1, and a paralogous ClpP5 gene was isolated and confirmed as the candidate for the vyl-modifier. Expression of Chr.1_ClpP5 is induced significantly in B73 by the vyl mutation, while the expression of Chr.1_ClpP5 in PH09B is not responsive to the vyl mutation. Moreover, expression and sequence analysis suggests that the PH09B Chr.1_ClpP5 allele is functionally weaker than the B73 allele. We propose that functional redundancy between duplicated paralogous genes is the molecular mechanism for the interaction between vyl and its modifier.

KEYWORDS:

Clp protease; Zea mays; background effect; duplicate genes; modifier; virescent yellow

PMID:
24888539
DOI:
10.1111/tpj.12568
[Indexed for MEDLINE]
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