Abstract
BackgroundThe Arabidopsis var2 mutant displays a unique green and white/yellow leaf variegation phenotype and lacks VAR2, a chloroplast FtsH metalloprotease. We are characterizing second-site var2 genetic suppressors as means to better understand VAR2 function and to study the regulation of chloroplast biogenesis.ResultsIn this report, we show that the suppression of var2 variegation in suppressor line TAG-11 is due to the disruption of the SUPPRESSOR OF VARIEGATION3 (SVR3) gene, encoding a putative TypA-like translation elongation factor. SVR3 is targeted to the chloroplast and svr3 single mutants have uniformly pale green leaves at 22°C. Consistent with this phenotype, most chloroplast proteins and rRNA species in svr3 have close to normal accumulation profiles, with the notable exception of the Photosystem II reaction center D1 protein, which is present at greatly reduced levels. When svr3 is challenged with chilling temperature (8°C), it develops a pronounced chlorosis that is accompanied by abnormal chloroplast rRNA processing and chloroplast protein accumulation. Double mutant analysis indicates a possible synergistic interaction between svr3 and svr7, which is defective in a chloroplast pentatricopeptide repeat (PPR) protein.ConclusionsOur findings, on one hand, reinforce the strong genetic link between VAR2 and chloroplast translation, and on the other hand, point to a critical role of SVR3, and possibly some aspects of chloroplast translation, in the response of plants to chilling stress.
Highlights
The Arabidopsis var2 mutant displays a unique green and white/yellow leaf variegation phenotype and lacks VAR2, a chloroplast FtsH metalloprotease
We show that suppression of var2 in this line is caused by disruption of SUPPRESSOR OF VARIEGATION3 (SVR3), a gene that encodes a chloroplast homolog of the E. coli TypA translation elongation factor
Analyses of F2 and F3 progeny from a cross between TAG-11 and var2-5 indicated that the suppression phenotype in TAG-11 is due to a recessive mutation that co-segregates with a complex T-DNA insertion pattern at a single locus (Additional file 1, Figure S1)
Summary
The Arabidopsis var mutant displays a unique green and white/yellow leaf variegation phenotype and lacks VAR2, a chloroplast FtsH metalloprotease. We are characterizing second-site var genetic suppressors as means to better understand VAR2 function and to study the regulation of chloroplast biogenesis. Variegation mutants are ideal models for studying the mechanisms of chloroplast biogenesis. The Arabidopsis variegation (var2) mutant displays green and white/yellow patches in normally green organs. The green sectors contain morphologically normal chloroplasts while the white sectors contain abnormal plastids that lack chlorophyll and contain underdeveloped lamellar structures [6,7]. The variegation phenotype of var is a recessive trait and is caused by the loss of a nuclear gene product for an FtsH ATP-dependent metalloprotease that is targeted to chloroplast thylakoid membranes [7,8]
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