Measuring the Effectiveness of Photoresponsive Nanocomposite Coatings on Aircraft Windshields to Mitigate Laser Intensity

In 2004, pilots reported 46 laser illumination events to the Federal Aviation Administration (FAA), with the number increasing to approximately 3,600 in 2011. Since that time, the number of reported laser incidents has ranged from 3,500 to 4,000. Previous studies indicate the potential for flight crewmember distraction from bright laser light being introduced to the cockpit. Compositional variations of the photoresponsive nanocomposite coatings were applied to an aircraft windscreen using a modified liquid dispersion/heating curing process. The attenuating effects of the deposited films on laser light intensity were evaluated using an optical power meter and the resultant laser intensity data through treated and untreated windscreens was collected. Data revealed a reduction in laser intensity (36–88%) in the presence of the engineered photoresponsive nanocomposite films. Results lend support of the view that the addition of transparent laser attenuating films applied to aircraft windscreens may improve flight safety, and reduce the risk from distraction or disruption of flight crewmembers’ vision

The Stress Response Factors Yap6, Cin5, Phd1, and Skn7 Direct Targeting of the Conserved Co-Repressor Tup1-Ssn6 in S. cerevisiae

Maintaining the proper expression of the transcriptome during development or in response to a changing environment requires a delicate balance between transcriptional regulators with activating and repressing functions. The budding yeast transcriptional co-repressor Tup1-Ssn6 is a model for studying similar repressor complexes in multicellular eukaryotes. Tup1-Ssn6 does not bind DNA directly, but is directed to individual promoters by one or more DNA-binding proteins, referred to as Tup1 recruiters. This functional architecture allows the Tup1-Ssn6 to modulate the expression of genes required for the response to a variety of cellular stresses. To understand the targeting or the Tup1-Ssn6 complex, we determined the genomic distribution of Tup1 and Ssn6 by ChIP-chip. We found that most loci bound by Tup1-Ssn6 could not be explained by co-occupancy with a known recruiting cofactor and that deletion of individual known Tup1 recruiters did not significantly alter the Tup1 binding profile. These observations suggest that new Tup1 recruiting proteins remain to be discovered and that Tup1 recruitment typically depends on multiple recruiting cofactors. To identify new recruiting proteins, we computationally screened for factors with binding patterns similar to the observed Tup1-Ssn6 genomic distribution. Four top candidates, Cin5, Skn7, Phd1, and Yap6, all known to be associated with stress response gene regulation, were experimentally confirmed to physically interact with Tup1 and/or Ssn6. Incorporating these new recruitment cofactors with previously characterized cofactors now explains the majority of Tup1 targeting across the genome, and expands our understanding of the mechanism by which Tup1-Ssn6 is directed to its targets