E. Lupotto

ABSTRACT An important goal in maize breeding is represented by the development of genotypes capable of maintaining competitive production yields in adverse as well as in optimal environments (Gardner and Stevens 1988; Stevens et al. 1988). Breeding maize solely for yield, in high-yielding environments, may lead to the loss of genes responsible for the buffer system of the plant toward stresses. Maize has been categorized among the crops most sensitive to salinity, and it is considered the most salt-sensitive species among cereals (Maas and Hoffmann 1977). Although maize cultivation is generally replaced in saline soils by more adapted crop systems, it would, however, be useful to explore the genetic diversity existing in maize germplasm for tolerance to salt. It is also well known that climatic and soil conditions may cause accumulation of salts also in areas in which this problem has never been encountered before (Epstein 1976). The capacity of a crop species to minimize the unfavorable effects elicited by salt is an important attribute advantageous for plant survival, development, and yield. The most relevant effect of salinity is a general growth retardation of the plant (Bernstein and Hayward 1958; Bernstein 1975). Plants like maize, in which yield is strongly linked to the vegetative dry matter production, suffer the salt effects mainly as decrease in plant size and consequent yield reduction (Bernstein 1964). Data available in literature strongly demonstrate the existence of a conspicuous genetic variability among maize genotypes in their capacity to buffer extreme conditions of the environment. The effects of salinity on some cultivars of maize grown in Pakistan have been recently investigated. The work performed on germination in the presence of NaCl, shows the existence of genetic variability for the trait of salt tolerance in the very early stages of growth (Ashraf and McNeilly 1986). The data analyzed, however, also point out that each genotype most likely displays its own independent mechanism for buffering the salt effects and that, in general, the whole plant performance in soil still gives the best selection criterion (e.g., Rush and Epstein 1981; Kingsbury and Epstein 1984).

ABSTRACT Small heat shock proteins in plants are produced under stress conditions and play an important role in stress tolerance. The gene Hvhsp17 isolated from barley encodes a class I, low molecular weight heat shock protein (or sHSP) which is induced in barley seedlings in response to heat stress. Previous molecular analysis of the 5′ promoter region of Hvhsp17 uncovered several cis regulatory elements upstream from the ATG of the gene, two heat shock elements (HSE1 and HSE2), and a sequence highly homologous to a metal responsive element of mammalian cells. The importance of the protective role of these elements against abiotic stresses was investigated both in barley and in maize. The expression profile of Hvhsp17 in response to various environmental conditions was analysed in these two cereals, to understand the regulation of Hvhsp17 gene expression and also in relation to conditions other than heat shock. The expression of Hvhsp17 in both barley and maize is strictly associated with heat stress, except for treatment with cadmium ions.

Polygalacturonase-inhibiting proteins (PGIPs), leucine-rich repeat (LRR) proteins evolutionarily related to several plant resistance genes, bind to and regulate the action of fungal endopolygalacturonases. In Phaseolus vulgaris L., PGIPs are encoded by a gene family comprising at least five members. As a start for a systematic analysis of the regulation of the pgip family, we have analysed the ability of the promoter of the bean gene pgip-1 to direct expression of beta-glucuronidase (GUS) in transfected tobacco protoplasts, microbombarded bean and tobacco leaves, and transgenic tobacco plants. In protoplasts, the pgip-1 gene region from nucleotide (nt) -2004 to nt +27 directed a level of expression that was as high as that directed by the cauliflower mosaic virus (CaMV) 35S promoter and could not be further induced by elicitor treatment; alteration of the region immediately following the TATAA sequence at nt -29 abolished expression. Upon stable integration into tobacco plants of the pgip-1 promoter-GUS construct, as well as of a -394 deletion, expression was detected for both constructs mainly in the stigma and, to a lesser extent, in the anthers and in the conductive vascular tissue. The promoter responded to wounding but not to oligogalacturonides, fungal glucan, salicylic acid, cryptogein, or pathogen infection. This expression pattern does not mirror that of the whole pgip gene family.