Mutations in the plant-conserved MTERF9 alter chloroplast gene expression, development and tolerance to abiotic stress in Arabidopsis thaliana.
The control of organelle gene expression in plants is far from fully understood. The characterization of mutants in Arabidopsis thaliana is assigning an increasingly prominent role to the mitochondrial transcription termination factors (mTERFs) in this process. To gain insight into the function of mTERF genes in plants, we took a reverse genetics approach to identify and characterize A. thaliana mTERF-defective mutants. Here we report the characterization of the mterf9 mutant, affected in an mTERF protein functionally conserved in plants and targeted to chloroplasts. Loss of MTERF9 results in defective chloroplast development, which is likely to cause paleness, stunted growth and reduced mesophyll cell numbers. Expression analysis of different plastid genes revealed reduced levels of plastid-encoded polymerase (PEP)-dependent transcripts and increased levels of transcripts dependent of nucleus-encoded polymerase. mterf9 plants exhibited altered responses to sugars, abscisic acid (ABA), salt and osmotic stresses, and the microarray data analysis showed modifications in MTERF9 expression after salt or mannitol treatments. Our genetic interactions results indicate a functional relationship between MTERF9 and the previously characterized MDA1 gene, and between MDA1 and some plastid ribosomal genes. MDA1 and MTERF9 were upregulated in the mterf9 and mda1 mutants, respectively. Moreover, 21 of 50 genes were commonly co-expressed with MDA1 and MTERF9. The analysis of the MDA1 and MTERF9 promoters showed that both were rich in stress-related cis-regulatory elements. Our results highlight the role of the MTERF9 gene in plant biology and deepens the understanding of the functional relationship of plant mTERF genes.
Instituto de Bioingeniería, Universidad Miguel Hernández, Elche 03202, Spain.
Pedro
P
Robles
Instituto de Bioingeniería, Universidad Miguel Hernández, Elche 03202, Spain.
José Luis
JL
Micol
Instituto de Bioingeniería, Universidad Miguel Hernández, Elche 03202, Spain.
Víctor
V
Quesada
D000040:Abscisic Acid / Q000494:pharmacology*; D017360:Arabidopsis / Q000235:genetics* / Q000254:growth & development / Q000502:physiology / Q000648:ultrastructure; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism; D002467:Cell Nucleus / Q000378:metabolism; D060365:Chloroplast Proteins / Q000235:genetics / Q000378:metabolism; D002736:Chloroplasts / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D008928:Mitochondria / Q000378:metabolism; D016254:Mutagenesis, Insertional; D009997:Osmotic Pressure; D010454:Peptide Termination Factors / Q000235:genetics / Q000378:metabolism; D010937:Plant Growth Regulators / Q000494:pharmacology*; D030821:Plants, Genetically Modified; D018087:Plastids / Q000378:metabolism*; D036226:Seedlings / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D012965:Sodium Chloride / Q000494:pharmacology; D013312:Stress, Physiological; D014157:Transcription Factors
D029681:Arabidopsis Proteins; C578065:At4g14605 protein, Arabidopsis; D060365:Chloroplast Proteins; C000605232:MTERF9 protein, Arabidopsis; D010454:Peptide Termination Factors; D010937:Plant Growth Regulators; D014157:Transcription Factors; D012965:Sodium Chloride; D000040:Abscisic Acid