Chlorophyll deficiency in the maize elongated mesocotyl2 mutant is caused by a defective heme oxygenase and delaying grana stacking.
Chlorophyll deficiency in the maize elongated mesocotyl2 mutant is caused by a defective heme oxygenase and delaying grana stacking.
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DOI:
10.1371/journal.pone.0080107
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Jin W
中科院分区:
文献类型:
--
作者:
Shi D;Zheng X;Li L;Lin W;Xie W;Yang J;Chen S;Jin W
Etiolated seedlings initiate grana stacking and chlorophyll biosynthesis in parallel with the first exposure to light, during which phytochromes play an important role. Functional phytochromes are biosynthesized separately for two components. One phytochrome is biosynthesized for apoprotein and the other is biosynthesized for the chromophore that includes heme oxygenase (HO). We isolated a ho1 homolog by map-based cloning of a maize elongated mesocotyl2 (elm2) mutant. cDNA sequencing of the ho1 homolog in elm2 revealed a 31 bp deletion. De-etiolation responses to red and far-red light were disrupted in elm2 seedlings, with a pronounced elongation of the mesocotyl. The endogenous HO activity in the elm2 mutant decreased remarkably. Transgenic complementation further confirmed the dysfunction in the maize ho1 gene. Moreover, non-appressed thylakoids were specifically stacked at the seedling stage in the elm2 mutant. The 31 bp deletion in the ho1 gene resulted in a decrease in endogenous HO activity and disrupted the de-etiolation responses to red and far-red light. The specific stacking of non-appressed thylakoids suggested that the chlorophyll biosynthesis regulated by HO1 is achieved by coordinating the heme level with the regulation of grana stacking.
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