95 publications from this institution
Functional markers for stress tolerance can be used in plant breeding to identify genotypes with high yield stabilities under various conditions. Thus, a good marker should show a strong correlation with favourable adaptive plant behaviour. The efficient reprogramming of target cells for yield determination is currently considered to be the most important step towards defining abiotic stress tolerance. In this Opinion article, we propose a role for the alternative oxidase (AOX) gene as a marker for genetic variation in cell reprogramming and yield stability. Evidence to support this idea comes from the metabolic role of alternative respiration under stress, the link between AOX activity and differential growth, and the single nucleotide polymorphism recently observed in AOX genes. We propose an innovative, interdisciplinary and global research strategy for future experimentation on AOX genes that could have an application in plant breeding.
Genome fingerprinting by random amplified polymorphic DNA (RAPD) is a subject for critical discussion. Reproducibility of the method is often hampered by its high sensitivity to experimental and technical conditions and generation of a fingerprint pattern is highly determined by competition between primer binding sites in the genome of interist. Nevertheless, under standardized conditions, the especially high sensitivity of genome organisation to RAPD analysis may particularly offer the chance to reveal differential changes in genome organisation using markers. To test this hypothesis, RAPD fingerprints were performed on a primary culture and on different tissues and organs of carrot plants, including leaves of different ages. Polymorphic RAPD bands were discovered that were dependent on the regulation of cell division-growth, displayed tissue specificity or depended on the age of the tissue. The differential RAPD fingerprints were reproducible and occurred with different individual plants of similar genotypes. The observed polymorphism was obviously based on quantitative variation in the target genomes. Also, the putative loss of variable bands could be traced back to quantitative polymorphism by varying primer or template concentration.
