Type Ia supernovae from violent mergers of carbon-oxygen white dwarfs: polarization signatures

The violent merger of two carbon-oxygen white dwarfs has been proposed as a viable progenitor for some Type Ia supernovae. However, it has been argued that the strong ejecta asymmetries produced by this model might be inconsistent with the low degree of polarization typically observed in Type Ia supernova explosions. Here, we test this claim by carrying out a spectropolarimetric analysis for the model proposed by Pakmor et al. for an explosion triggered during the merger of a 1.1 and 0.9 M⊙ carbon-oxygen white dwarf binary system. Owing to the asymmetries of the ejecta, the polarization signal varies significantly with viewing angle. We find that polarization levels for observers in the equatorial plane are modest (≲1 per cent) and show clear evidence for a dominant axis, as a consequence of the ejecta symmetry about the orbital plane. In contrast, orientations out of the plane are associated with higher degrees of polarization and departures from a dominant axis. While the particular model studied here gives a good match to highly polarized events such as SN 2004dt, it has difficulties in reproducing the low polarization levels commonly observed in normal Type Ia supernovae. Specifically, we find that significant asymmetries in the element distribution result in a wealth of strong polarization features that are not observed in the majority of currently available spectropolarimetric data of Type Ia supernovae. Future studies will map out the parameter space of the merger scenario to investigate if alternative models can provide better agreement with observations.

EspZ of enteropathogenic and enterohemorrhagic Escherichia coli regulates type III secretion system protein translocation

UNLABELLED: Translocation of effector proteins via a type III secretion system (T3SS) is a widespread infection strategy among Gram-negative bacterial pathogens. Each pathogen translocates a particular set of effectors that subvert cell signaling in a way that suits its particular infection cycle. However, as effector unbalance might lead to cytotoxicity, the pathogens must employ mechanisms that regulate the intracellular effector concentration. We present evidence that the effector EspZ controls T3SS effector translocation from enteropathogenic (EPEC) and enterohemorrhagic (EHEC) Escherichia coli. Consistently, an EPEC espZ mutant is highly cytotoxic. Following ectopic expression, we found that EspZ inhibited the formation of actin pedestals as it blocked the translocation of Tir, as well as other effectors, including Map and EspF. Moreover, during infection EspZ inhibited effector translocation following superinfection. Importantly, while EspZ of EHEC O157:H7 had a universal "translocation stop" activity, EspZ of EPEC inhibited effector translocation from typical EPEC strains but not from EHEC O157:H7 or its progenitor, atypical EPEC O55:H7. We found that the N and C termini of EspZ, which contains two transmembrane domains, face the cytosolic leaflet of the plasma membrane at the site of bacterial attachment, while the extracellular loop of EspZ is responsible for its strain-specific activity. These results show that EPEC and EHEC acquired a sophisticated mechanism to regulate the effector translocation.

IMPORTANCE: Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) are important diarrheal pathogens responsible for significant morbidity and mortality in developing countries and the developed world, respectively. The virulence strategy of EPEC and EHEC revolves around a conserved type III secretion system (T3SS), which translocates bacterial proteins known as effectors directly into host cells. Previous studies have shown that when cells are infected in two waves with EPEC, the first wave inhibits effector translocation by the second wave in a T3SS-dependent manner, although the factor involved was not known. Importantly, we identified EspZ as the effector responsible for blocking protein translocation following a secondary EPEC infection. Interestingly, we found that while EspZ of EHEC can block protein translocation from both EPEC and EHEC strains, EPEC EspZ cannot block translocation from EHEC. These studies show that EPEC and EHEC employ a novel infection strategy to regulate T3SS translocation.