No abstract

The penetration of diesel particulate filters (DPFs) in the market is growing fast. However, in the current inspection/maintenance (I/M) regulation for these vehicles, particulate emissions were capped with smoke opacity, which is incompetent to identify the excessive particle number (PN) induced by non-major DPF failures such as small cracks in substrate. This research aimed at developing a fast identification method for such malfunctioning vehicles using a low-cost condensation particle counter (CPC). To verify the effectiveness of idle PN test, 33 China-5 and China-6 heavy-duty vehicles fueled with diesel and natural gas (NG) were tested using the regulatory portable emission measurement system (PEMS) as per China-6 protocol and idle PN tests using a low-cost CPC-based system. PN emissions from China-6 vehicles with malfunctioning DPFs were at a similar level to those from China-5 vehicles (without DPF), which were significantly higher than the proper counterparts. Idle PN tests using a CPC-based system managed to identify the vehicles with DPF failures. Volumetric PN concentrations of these vehicles were much higher than those of the proper ones. This study proved that an easy, fast, and low-cost procedure could be used to screen out those high emitters with DPF failure.

No abstract

CRISPR-Cas system provides prokaryotes with protection against mobile genetic elements (MGEs) such as phages. In turn, phages deploy anti-CRISPR (Acr) proteins to evade this immunity. AcrIF4, an Acr targeting the type I-F CRISPR-Cas system, has been reported to bind the crRNA-guided surveillance (Csy) complex. However, it remains controversial whether AcrIF4 inhibits target DNA binding to the Csy complex. Here, we present structural and mechanistic studies into AcrIF4, exploring its unique anti-CRISPR mechanism. While the Csy-AcrIF4 complex displays decreased affinity for target DNA, it is still able to bind the DNA. Structural and functional analyses of the Csy-AcrIF4-dsDNA complex revealed that AcrIF4 binding prevents rotation of the helical bundle (HB) of Cas8f induced by dsDNA binding, therefore resulting in failure of Cas2/3 recruitment and DNA cleavage. Overall, our study provides an interesting example of attack on the nuclease recruitment event by an Acr, but not conventional mechanisms of blocking binding of target DNA.