Light controls many processes in filamentous fungi. The study of light regulation in a number of model organisms revealed an unexpected complexity. Although the molecular components for light sensing appear to be widely conserved in fungal genomes, the regulatory circuits and the sensitivity of certain species toward specific wavelengths seem different. In N. crassa , most light responses are triggered by blue light, whereas in A. nidulans , red light plays a dominant role. In Alternaria alternata , both blue and red light appear to be important. In A. alternata , photoreceptors control morphogenetic pathways, the homeostasis of reactive oxygen species, and the production of secondary metabolites. On the other hand, high-osmolarity sensing required FphA and LreA, indicating a sophisticated cross talk between light and stress signaling.

Fungi sense light of different wavelengths using blue-, green-, and red-light photoreceptors. Blue light sensing requires the “white-collar” proteins with flavin as chromophore, and red light is sensed through phytochrome. Here we analyzed genome-wide gene expression changes caused by short-term, low-light intensity illumination with blue-, red- or far-red light in Aspergillus nidulans and found that more than 1100 genes were differentially regulated. The largest number of up- and downregulated genes depended on the phytochrome FphA and the attached HOG pathway. FphA and the white-collar orthologue LreA fulfill activating but also repressing functions under all light conditions and both appear to have roles in the dark. Additionally, we found about 100 genes, which are red-light induced in the absence of phytochrome, suggesting alternative red-light sensing systems. We also found blue-light induced genes in the absence of the blue-light receptor LreA. We present evidence that cryptochrome may be part of this regulatory cue, but that phytochrome is essential for the response. In addition to in vivo data showing that FphA is involved in blue-light sensing, we performed spectroscopy of purified phytochrome and show that it responds indeed to blue light.

Aims: To investigate the prevalence of acquired multidrug resistance of P. aeruginosa among clinical samples obtained from patients attending Ekiti State University Teaching Hospital, Ado Ekiti, Ekiti State, Nigeria. Place and Duration of Study: Ekiti State Teaching Hospital from January-March 2013. Methodology: The isolates were characterized by standard cultural and biochemical tests and they were tested for their sensitivity to different antibiotics using disk diffusion method. Results: A total of 192 clinical samples were collected from which 42 isolates of P. aeruginosa were obtained. Antibiogram profile showed that a total of 80.95% of the isolates were resistant to ceftriaxone and ceftizoxime respectively, 76.2% to augmentin, 73.8% to ceftazidime, 71.4% to nitrofurantoin, 47.6% to ofloxacin, 45.23% to gentamicin while ciprofloxacin had the lowest resistance of 42.86. Isolates from ear swabs had the highest resistance to 3^rd generation cephalosporins, followed by isolates from urine while isolates from wound samples showed the lowest resistance. Conclusion: There is a need to institute an effective antimicrobial resistance surveillance system that provides clinicians with up-to-date data on the prevalence and resistance pattern of commonly encountered pathogens like P. aeruginosa especially as nosocomial infection is concerned.

In the comparative transcriptomic studies of wild type (WT) and rax1 null mutant strains, we obtained an average of 22,222,727 reads of 101 bp per sample and found that 183 genes showed greater than 2.0-fold differential expression, where 92 and 91 genes were up-and down-regulated in Δrax1 compared to WT, respectively. In accordance with the significantly reduced levels of gliM and casB transcripts in the absence of rax1, the Δrax1 mutant exhibited increased sensitivity to exogenous gliotoxin (GT) without affecting levels of GT production. Moreover, Δrax1 resulted in significantly restricted colony growth and reduced viability under endoplasmic reticulum stress condition. In summary, Rax1 positively affects expression of gliM and metacaspase genes.