Possibilities for using molecular markers to improve genebank efficiency are increasingly present thanks to developments in genebanks and developments in molecular genetics. These possibilities relate to all aspects of genebank management: acquisition, maintenance, characterisation and utilisation. However, two pitfalls should be avoided. The first lies in the neutrality of the most generally used markers, making them less suitable for optimising genetic diversity. The second is related to the considerable costs involved in using molecular markers. In many cases an economical analysis will have to decide if the markers can routinely be used in genebank operations. Some examples of model studies and applications of molecular markers in genebank operations will be presented, in which both genetic and economic aspects will be illustrated briefly. These examples involved existing genebank collections of wild lettuce, cabbage and wild potato.
The mechanical properties of the red cell are accounted for by its membrane and its membrane skeleton, the latter being a protein network that laminates the inner surface of the lipid bilayer. Hereditary spherocytosis (HS) is the most common of congenital hemolytic anemias. The spherocytes have a reduced lifespan due to their spheroidal shape that alters their resistance and elastic deformability. It is now established that the responsible alterations affect most often the ANK1 gene that encodes erythroid ankyrin. A noticeable HS subset is associated with a reduction of the anion exchanger 1 (AE1, or band 3), due to mutation in the corresponding gene, the EPB3 gene. Much more rarely, HS goes along with a sharp reduction, if not the absence, of protein 4.2. This stigmata results either from mutations in the DNA sequences that encode the binding site of the AE1 cytoplasmic domain for protein 4.2, or from mutations of protein 4.2 gene itself, the ELP42 gene. Mutations responsible for HS lie rarely or exceptionally in the spectrin β- or the α-genes (SPTB and SPTA1 genes, respectively). Elucidation of new HS mutations is presently at its height. It casts light on the function of specific domains within the various proteins involved, and on the integration of protein structure and function at the cellular scale.
Salinity in soil affects about 7 % of the land’s surface and about 5 % of cultivated land. Most importantly, about 20 % of irrigated land has suffered from secondary salinisation and 50 % of irrigation schemes are affected by salts. In many hotter, drier countries of the world salinity is a concern in their agriculture and could become a key issue. Consequently, the development of salt resistant crops is seen as an important area of research. Although there has been considerable research into the effects of salts on crop plants, there has not, unfortunately, been a commensurate release of salt tolerant cultivars of crop plants. The reason is likely to be the complex nature of the effect of salts on plants. Given the rapid increase in molecular biological techniques, a key question is whether such techniques can aid the development of salt resistance in plants. Physiological and biochemical research has shown that salt tolerance depends on a range of adaptations embracing many aspects of a plant’s physiology: one of these the compartmentation of ions. Introducing genes for compatible solutes, a key part of ion compartmentation, in salt-sensitive species is, conceptually, a simple way of enhancing tolerance. However, analysis of the few data available suggests the consequences of transformation are not straightforward. This is not unexpected for a multigenic trait where the hierarchy of various aspects of tolerance may differ between and within species. The experimental evaluation of the response of transgenic plants to stress does not always match, in quality, the molecular biology. We have advocated the use of physiological traits in breeding programmes as a process that can be undertaken at the present while more knowledge of the genetic basis of salt tolerance is obtained. The use of molecular biological techniques might aid plant breeders through the development of marker aided selection.
The study of candidate genes, based on physiological effects, is an important tool to identify genes to be used in marker-assisted selection programs. In this study, a group of halothane gene-free, non-castrated, male Landrace pigs was used to study the association between polymorphisms in the PIT1 (n = 218), GH (n = 213) and GHRH (n = 206) genes and fat thickness, average daily gain, and the EPD (expected progeny difference) for fat thickness, average daily gain, and litter size. These genes are potential candidate markers because of their important physiological effects. The pigs were genotyped by PCR-RFLP, and the statistical model used to analyze the association between genotypes and the traits measured included genotypes as a fixed effect and age and weight as covariates. PIT1 polymorphisms were associated with fat thickness (P = 0.0019), EPD for average daily gain (P = 0.0001) and EPD for fat thickness (P = 0.0001), whereas GH polymorphisms were associated with fat thickness (P = 0.0326) and average daily gain (P = 0.0127), and GHRH polymorphisms were associated with the average daily gain (P = 0.0001) and EPD for fat thickness (P = 0.0004). These results confirmed the potential usefulness of these genes in marker-assisted selection programs for pig breeding.
Although it is estimated that 20-30% of the general human population are carriers of Staphylococcus aureus, this bacterium is one of the most important etiological agents responsible for healthcare-associated infections. The appearance of methicillin resistant S. aureus (MRSA) strains has created serious therapeutical problems. Detailed understanding of the mechanisms of S. aureus infections seems necessary to develop new effective therapies against this pathogen. In this article, we present an overview of the biochemical and genetic mechanisms of pathogenicity of S. aureus strains. Virulence factors, organization of the genome and regulation of expression of genes involved in virulence, and mechanisms leading to methicilin resistance are presented and briefly discussed.