Journal of Stress Physiology & Biochemistry, Vol. 12 No. 1 2016, pp. 108-118  ISSN 1997-0838
Original Text Copyright (cc) 2015 by  Yakovleva, Zubo, Tarasenko, Garnik, Borner and Konstantinov



ORIGINAL ARTICLE
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Effect of Photosynthetic Electron Transport Inhibition in vivo on the Chloroplast Genes Transcription in Arabidopsis

T.V. Yakovleva1, Y.O. Zubo2, V.I. Tarasenko1, E.Yu. Garnik1*, T. Borner2, Yu.M. Konstantinov1

1  Siberian Institute of Plant Physiology and Biochemistry, SB RAS, Irkutsk, Russia
2  Institute of Biology-Genetics, Humboldt University, Berlin, Germany

*E-Mail: elga74@yandex.ru

Received January 25, 2016

Transcription of both nuclear and plastid genes encoding components of photosynthetic apparatus is subjected to redox regulation. The origin of redox signals mediating this regulation is chloroplast electron transport chain (ETC) itself. Up to date the effects of redox state of individual ETC components on chloroplast genes transcription rate was demonstrated only for some selected genes and only in isolated chloroplasts. In the present work ETC inhibitors was used for in vivo modulations in plastoquinone pool redox state, and run-on transcription approach was used to evaluate the plastid genes transcription rate. We have demonstrated that plastoquinone redox state has impact on transcription rate of wide range of Arabidopsis chloroplast genes. Treatment by DCMU (plastoquinone pool is oxidized) lead to increase of transcription rate of the majority of plastid genes studied. Treatment by DBMIB (plastoquinone pool is reduced) lead to decrease of plastid genes transcription rate. Simultaneous treatment by one of photosynthesis inhibitors and KCN (mitochondrial respiratory complex IV inhibitor) lead to decrease of transcription rate of plastid genes in most cases. Our results suggest probable participation of mitochondria in the redox regulation of plastid genes expression in Arabidopsis.


Key words:   
Arabidopsis thaliana, plastid genes expression, photosynthetic electron transport, DCMU, DBMIB


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