Azollais a floating pteridophyte, which contains as endosymbiont the nitrogen-fixing cyanobacteriumAnabaena azollae(Nostocaceae family). Widely cultivated in the Asian regions,Azollais either incorporated into the soil before rice transplanting or grown as a dual crop along with rice. To examine the feasibility of its use in flooded rice fields sited in the Temperate European Areas, we carried out a series of experiments in PVC tanks during 2000–2002 in Po Valley (northern Italy) conditions, to study the growth-development dynamics and the resistance/tolerance to low temperatures and to commonly used herbicides of several differentAzollastrains. Three out of five strains tested survived the winter, with an increase in biomass from March to May producing approximately 30–40 kg of nitrogen. One of these strains, named “Milan”, emerged as the most resistant to herbicide and the most productive. Of the herbicides tested, Propanil permitted the survival of growingAzolla.
In maize vivipary, the precocious germination of the seed while still attached to the ear, is the diagnostic phenotype of mutants, which are impaired in the biosynthesis or response to abscisic acid (ABA). Of the 15 genes so far described, 12 control specific steps in ABA biosynthesis, two mediate hormone response and one still has an undefined role. We have analyzed a collection of 25 independent vp isolates with the aim of determining the degree of mutational saturation that has so far been reached. Of the 25 viviparous mutants complementation tested, 22 correspond to known loci: six are allelic to vp1, another six to vp5, one to vp7, two to vp9, six to vp10 and one to w3. The remaining three represent genes not previously identified. All mutants so far tested except rea show a decrease in ABA content. As to the only two mutants (vp1 and rea) whose endogenous ABA content is not impaired, the reduction in sensitivity of the double mutant compared to the single ones suggests that the two genes control separate pathways in the ABA signal transduction. Some of the mutants in this collection have a characteristic incomplete germination that allows the embryo of the mature dry seed to resume germination. By exploiting this feature it is possible to infer, through a germination test, whether the mutant has been impaired in the acquisition of desiccation tolerance. This information provides the starting point for the dissection of the genetic basis of desiccation tolerance.
The maize seed comprises two major compartments, the embryo and the endosperm, both originating from the double fertilization event. The embryogenetic process allows the formation of a well-differentiated embryonic axis, surrounded by a single massive cotyledon, the scutellum. The mature endosperm constitutes the bulk of the seed and comprises specific regions containing reserve proteins, complex carbohydrates, and oils. To gain more insight into molecular events that underlie seed development, three monogenic mutants were characterized, referred to as emp (empty pericarp) on the basis of their extreme endosperm reduction, first recognizable at about 12 d after pollination. Their histological analysis reveals a partial development of the endosperm domains as well as loss of adhesion between pedicel tissues and the basal transfer layer. In the endosperm, programmed cell death (PCD) is delayed. The embryo appears retarded in its growth, but not impaired in its morphogenesis. The mutants can be rescued by culturing immature embryos, even though the seedlings appear retarded in their growth. The analysis of seeds with discordant embryo-endosperm phenotype (mutant embryo, normal endosperm and vice-versa), obtained using B-A translocations, suggests that emp expression in the embryo is necessary, but not sufficient, for proper seed development. In all three mutants the picture emerging is one of a general delay in processes related to growth, as a result of a mutation affecting endosperm development as a primary event.
In maize vivipary, the precocious germination of the seed while it is still attached to the ear is a reliable phenotype for the identification of mutants impaired in the biosynthesis or response to abscisic acid (ABA). Here we present the characterization of a new allele of vp10, a gene encoding for a cofactor (MoCo) required for the last step of ABA biosynthesis. The lesion in this gene leads to a reduction in the endogenous ABA level. Embryonic messenger RNAs of the ABA inducible genes glb1, lea3, and rab17 are barely detectable, although their level increases when stimulated by exogenous ABA administration. These findings confirm that the mutant can be ascribed to a defect in ABA biosynthesis. In the absence of water stress, mutant plants grow like wild-type siblings; however when mutant tissues are exposed to air they differ from non-mutant ones by showing a higher rate of water loss, of transpiration and of stomatal conductance. These events are restored to almost normal values by adding exogenous ABA. All these defects are ascribable to an impairment in the regulation of stomatal opening since, in contrast to wild-type, some of the mutant stomata exhibit partially or totally open rims. The defect in ABA biosynthesis is also associated with loss of regulation of the expression of rab17 and rab28, two genes expressed in vegetative tissues under abiotic stress. These genes are constitutively expressed in the mutant plant tissues independently of the water regime applied. Thus this mutant may provide a tool for the study of molecular mechanisms underlying drought-stress responses in crop plants
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