SummaryThe role of the Arabidopsis transcription factor LONG HYPOCOTYL 5 (HY5) in promoting photomorphogenic development has been extensively characterized. Although the current model for HY5 action largely explains its role in this process, it does not adequately address the root phenotype observed in hy5 mutants. In our search for common mechanisms underlying all hy5 traits, we found that they are partly the result of an altered balance of signaling through the plant hormones auxin and cytokinin. hy5 mutants are resistant to cytokinin application, and double mutant analyses indicate that a decrease in auxin signaling moderates hy5 phenotypes. Microarray analyses and semiquantitative RT-PCR indicate that two negative regulators of auxin signaling, AUXIN RESISTANT 2 (AXR2)/INDOLE ACETIC ACID 7 (IAA7) and SOLITARY ROOT (SLR)/IAA14, are underexpressed in hy5 mutants. The promoters of these genes contain a putative HY5 binding site, and in line with this observation, HY5 can bind to the promoter of AXR2 in vitro. Increased AXR2 expression in a hy5 background partially rescues the elongated hypocotyl phenotype. In summary, it appears that auxin signaling is elevated in hy5 mutants because HY5 promotes the expression of negative regulators of auxin signaling, thereby linking hormone and light signaling pathways.
Coenzyme Q10 has emerged as a valuable molecule for pharmaceutical and cosmetic applications. Therefore, research into producing and optimizing coenzyme Q10 via microbial fermentation is ongoing. There are two major paths being explored for maximizing production of this molecule to commercially advantageous levels. The first entails using microbes that naturally produce coenzyme Q10 as fermentation biocatalysts and optimizing the fermentation parameters in order to reach industrial levels of production. However, the natural coenzyme Q10-producing microbes tend to be intractable for industrial fermentation settings. The second path to coenzyme Q10 production being explored is to engineer Escherichia coli with the ability to biosynthesize this molecule in order to take advantage of its more favourable fermentation characteristics and the well-understood array of genetic tools available for this bacteria. Although many studies have attempted to over-produce coenzyme Q10 in E. coli through genetic engineering, production titres still remain below those of the natural coenzyme Q10-producing microorganisms. Current research is providing the knowledge needed to alleviate the bottlenecks involved in producing coenzyme Q10 from an E. coli strain platform and the fermentation parameters that could dramatically increase production titres from natural microbial producers. Synthesizing the lessons learned from both approaches may be the key towards a more cost-effective coenzyme Q10 industry.
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