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Published on January 23, 2003; 10.1104/pp.014530

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Received September 12, 2002
Returned for revision October 17, 2002
Accepted November 5, 2002

cor Gene Expression in Barley Mutants Affected in Chloroplast Development and Photosynthetic Electron Transport

Cristina Dal Bosco , Marco Busconi , Chiara Govoni , Paolo Baldi , A. Michele Stanca , Cristina Crosatti , Roberto Bassi , and Luigi Cattivelli *

Istituto Sperimentale per la Cerealicoltura, Via S. Protaso 302, I-29017, Fiorenzuola d'Arda (PC), Italy (C.D.B., M.B., C.G., P.B., A.M.S., C.C., L.C.); and Università di Verona, Facoltà di Scienze Matematiche Fisiche Naturali; Biotecnologie Vegetali, Strada Le Grazie, 37134, Verona, Italy (C.B.D., C.G., R.B.)

* Corresponding author; email: l.cattivelli{at}iol.it.

The expression of several barley (Hordeum vulgare) cold-regulated (cor) genes during cold acclimation was blocked in the albino mutant an, implying a chloroplast control on mRNAs accumulation. By using albino and xantha mutants ordered according to the step in chloroplast biogenesis affected, we show that the cold-dependent accumulation of cor14b, tmc-ap3, and blt14 mRNAs depends on plastid developmental stage. Plants acquire the ability to fully express cor genes only after the development of primary thylakoid membranes in their chloroplasts. To investigate the chloroplast-dependent mechanism involved in cor gene expression, the activity of a 643-bp cor14b promoter fragment was assayed in wild-type and albino mutant an leaf explants using transient {beta}-glucuronidase reporter expression assay. Deletion analysis identified a 27-bp region between nucleotides -274 and -247 with respect to the transcription start point, encompassing a boundary of some element that contributes to the cold-induced expression of cor14b. However, cor14b promoter was equally active in green and in albino an leaves, suggesting that chloroplast controls cor14b expression by posttranscriptional mechanisms. Barley mutants lacking either photosystem I or II reaction center complexes were then used to evaluate the effects of redox state of electron transport chain components on COR14b accumulation. In the mutants analyzed, the amount of COR14b protein, but not the steady-state level of the corresponding mRNA, was dependent on the redox state of the electron transport chain. Treatments of the vir-zb63 mutant with electron transport chain inhibitors showed that oxidized plastoquinone promotes COR14b accumulation, thus suggesting a molecular relationship between plastoquinone/plastoquinol pool and COR14b.




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