Fault Tolerance Analysis and Self-Healing Strategy of Autonomous, Evolvable Hardware Systems

This paper presents an analysis of the fault tolerance achieved by an autonomous, fully embedded evolvable hardware system, which uses a combination of partial dynamic reconfiguration and an evolutionary algorithm (EA). It demonstrates that the system may self-recover from both transient and cumulative permanent faults. This self-adaptive system, based on a 2D array of 16 (4×4) Processing Elements (PEs), is tested with an image filtering application. Results show that it may properly recover from faults in up to 3 PEs, that is, more than 18% cumulative permanent faults. Two fault models are used for testing purposes, at PE and CLB levels. Two self-healing strategies are also introduced, depending on whether fault diagnosis is available or not. They are based on scrubbing, fitness evaluation, dynamic partial reconfiguration and in-system evolutionary adaptation. Since most of these adaptability features are already available on the system for its normal operation, resource cost for self-healing is very low (only some code additions in the internal microprocessor core)

The Agrobacterium vitis T-6b oncoprotein induces auxin-independent cell expansion in tobacco

Among the Agrobacterium T-DNA genes, rolB, rolC, orf13, orf8, lso, 6b and several other genes encode weakly homologous proteins with remarkable effects on plant growth. The 6b oncogene induces tumors and enations. In order to study its properties we have used transgenic tobacco plants that carry a dexamethasone-inducible 6b gene, dex-T-6b. Upon induction, dex-T-6b plants develop a large array of morphological modifications, some of which involve abnormal cell expansion. In the present investigation, dex-T-6b-induced expansion was studied in intact leaves and an in vitro leaf disc system. Although T-6b and indole-3-acetic acid (IAA) both induced expansion and were non-additive, T-6b expression did not increase IAA levels, nor did it induce an IAA-responsive gene. Fusicoccin (FC) is known to stimulate expansion by increasing cell wall plasticity. T-6b- and FC-induced expansion were additive at saturating FC concentrations, indicating that T-6b does not act by a similar mechanism to FC. T-6b expression led to higher leaf osmolality values, in contrast to FC, suggesting that the T-6b gene induces expansion by increasing osmolyte concentrations. Metabolite profiling showed that glucose and fructose played a major role in this increase. We infer that T-6b disrupts the osmoregulatory controls that govern cell expansion during development and wound healing.