Proceedings of the XLVI Italian Society of Agricultural Genetics - SIGA Annual Congress

Giardini Naxos, Italy - 18/21 September, 2002

ISBN 88-900622-3-1

Oral Communication Abstract - S1c

ABIOTIC AND BIOTIC STRESS FACTORS AFFECT THE GERANYL GERANYL HYDROGENASE EXPRESSION IN PEACH LEAVES (PRUNUS PERSICA [L.] BATSCH)

GIANNINO D.*, CONDELLO E.**, BRUNO L.***, TESTONE G. **, COZZA R.***, TARTARINI A**, NICOLODI C.**, BITONTI M.B.***, INNOCENTI A.M.***, MARIOTTI D.**

*) Istituto per la Protezione delle Piante – Sezione di Bari, CNR, Via Amendola trav.147,16815 Bari

**) Istituto di Biologia Agro-ambientale e Forestale. Sezione di Roma, CNR, Via Salaria km 29,300, 00016 Monterotondo Scalo, Roma, Tel 06 90672539 Fax 06 9064492

mari@mlib.cnr.it

***) Dipartimento di Ecologia dell’Università della Calabria, Ponte Bucci, 87030 Arcavacata di Rende, Cosenza, Tel 0984 492965, Fax 0984 492964

b.bitonti@unical.it

peach, geranyl geranyl hydrogenase, stress response

A previous research showed that the gene encoding geranyl geranyl reductase (GGH), a key enzyme of the chlorophyll and tocopherol pathways, was regulated at the developmental level in peach leaves. In this work, GGH expression was monitored in response to light absence, cold treatment, wound injury and during the leaf curl disease, caused by the fungus Taphrina deformans. Mature and young leaves were subjected to dark and GGH messages appeared to decrease after 12 hrs, but they partially recovered with respect to controls in long last treatments (36 hrs). A similar pattern was observed in mechanically injured leaves, which exhibited a rapid decrease and recovery of GGH messages within only four hours from the treatment. Moreover, in plants maintained at 4°C, after growth chamber acclimation, leaf GGH expression was progressively down regulated within 24 hours. In curled leaves message decrease was tightly related to the damage intensity. Interestingly, in situ experiments revealed a strong transcript accumulation in distinct leaf portions at the early symptoms of disease. This pattern suggested that GGH was locally triggered in response to the pathogen induced oxidative stress by taking part in the tocopherol pathway.