Mutual influences of Pseudomonas aeruginosa and Desulfovibrio desulfuricans on their adhesion to stainless steel

The mutual influences of Pseudomonas aeruginosa PAO1 and Desulfovibrio desulfuricans subsp. desulfuricans (ATCC 29577) on their adhesion to stainless steel were investigated in batch and column experiments. It was found that P. aeruginosa promoted the adhesion of D. desulfuricans under conditions of turbulence, but not under quiescent conditions. The enhancement involved the alignment of most D. desulfuricans along P. aeruginosa cells and was attributed to the additional interaction surface area provided by adhered P. aeruginosa to aligning D. desulfuricans cells. A slightly positive effect of preadhered D. desulfuricans on the adhesion of P. aeruginosa was found. Under condition of laminar flow, substantially better adhesion of D. desulfuricans to confluent P. aeruginosa biofilms than to steel was observed. The mutual influences are discussed in terms of more favorable adhesion energies and the influence of changed hydraulic conditions due to the roughness of P. aeruginosa biofilms.     

Activation of the cAMP pathway in Ustilago maydis reduces fungal proliferation and teliospore formation in plant tumors

In the corn smut fungus Ustilago maydis, mating of two haploid sporidia is a prerequisite for subsequent colonization of the host. Cyclic AMP (cAMP) and pheromone signals have been implicated in this developmental program. The cAMP pathway is also needed for subsequent fungal development in planta, as null mutants in any component of the pathway fail to form tumors. Here we show that moderate activation of the pathway conferred either by mutation in the Galpha subunit or by mutation in the regulatory subunit of the protein kinase A influences tumor morphology. In the resulting tumors, the amount of fungal material is drastically reduced and fungal development is arrested at the stage of sporogenic hyphae. We conclude that tight regulation of the cAMP pathway is crucial for fungal development within the plant but does not interfere with the tumor induction process.     

Phenology in central Europe – differences and trends of spring phenophases in urban and rural areas

In order to examine the impacts of both large-scale and small-scale climate changes (urban climate effect) on the development of plants, long-term observations of four spring phenophases from ten central European regions (Hamburg, Berlin, Cologne, Frankfurt, Munich, Prague, Vienna, Zurich, Basle and Chur) were analysed. The objective of this study was to identify and compare the differences in the starting dates of the pre-spring phenophases, the beginning of flowering of the snowdrop (Galanthus nivalis) and forsythia (Forsythia sp.), and of the full-spring phenophases, the beginning of flowering of the sweet cherry (Prunus avium) and apple (Malus domestica), in urban and rural areas. The results indicate that, despite regional differences, in nearly all cases the species studied flower earlier in urbanised areas than in the corresponding rural areas. The forcing in urban areas was about 4 days for the pre-spring phenophases and about 2 days for the full-spring phenophases. The analysis of trends for the period from 1951 to 1995 showed tendencies towards an earlier flowering in all regions, but only 22% were significant at the 5% level. The trends for the period from 1980 to 1995 were much stronger for all regions and phases: the pre-spring phenophases on average became earlier by 13.9 days/decade in the urban areas and 15.3 days/decade in the rural areas, while the full-spring phenophases were 6.7 days earlier/decade in the urban areas and 9.1 days/decade earlier in the rural areas. Thus rural areas showed a higher trend towards an earlier flowering than did urban areas for the period from 1980 to 1995. However, these trends, especially for the pre-spring phenophases, turned out to be extremely variable. Received: 21 October 1999 / Revised: 5 April 2000 / Accepted: 25 April 2000     

Tim23 links the inner and outer mitochondrial membranes

Tim23, a key component of the mitochondrial preprotein translocase, is anchored in the inner membrane by its C-terminal domain and exposes an intermediate domain in the intermembrane space that functions as a presequence receptor. We show that the N-terminal domain of Tim23 is exposed on the surface of the outer membrane. The two-membrane-spanning topology of Tim23 is a novel characteristic in membrane biology. By the simultaneous integration into two membranes, Tim23 forms contacts between the outer and inner mitochondrial membranes. Tethering the inner membrane translocase to the outer membrane facilitates the transfer of precursor proteins from the TOM complex to the TIM23 complex and increases the efficiency of protein import.     

A fluorescently-labelled r-RNA targeted oligonucleotide probe for the in situ detection of G-bacteria of the genus Amaricoccus in activated sludge

A fluorescently-labelled r-RNAtargeted oligonucleotide probe specific for members of the genus Amaricoccus, which includes one group of the Gram-negative G-Bacteria seen in activated sludge systems, is described. These organisms, previously 'identified' on their distinctive morphology of cocci in tetrads, have been associated with poor performance of biological nutrient removal (EBNR) plants, by out-competing the polyphosphate accumulating bacteria. Methods of sample preparation for probing activated sludge are detailed, and preliminary surveys of 46 plants, using this probe, show that G-Bacteria belonging to the genus Amaricoccus are seen not only in large numbers in EBNR systems but also in conventional plants. The presence of single cells of this organism was common, emphasizing the dangers of relying on morphology and cell arrangement to identify these bacteria.     

Heterogeneous expression of ACE2 and TMPRRS2 in mesenchymal stromal cells

The outbreak of COVID‐19 has become a serious public health emergency. The virus targets cells by binding the ACE2 receptor. After infection, the virus triggers in some humans an immune storm containing the release of proinflammatory cytokines and chemokines followed by multiple organ failure. Several vaccines are enrolled, but an effective treatment is still missing. Mesenchymal stem cells (MSCs) have shown to secrete immunomodulatory factors that suppress this cytokine storm. Therefore, MSCs have been suggested as a potential treatment option for COVID‐19. We report here that the ACE2 expression is minimal or nonexistent in MSC derived from three different human tissue sources (adipose tissue, umbilical cord Wharton`s jelly and bone marrow). In contrast, TMPRSS2 that is implicated in SARS‐CoV‐2 entry has been detected in all MSC samples. These results are of particular importance for future MSC‐based cell therapies to treat severe cases after COVID‐19 infection.     

TRAIL induces apoptosis but not necroptosis in colorectal and pancreatic cancer cells preferentially via the TRAIL-R2/DR5 receptor

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine that can trigger apoptosis in many types of human cancer cells via engagement of its two pro-apoptotic receptors TRAIL-R1 (DR4) and TRAIL-R2 (DR5). TRAIL can also activate several other signaling pathways such as activation of stress kinases, canonical NF-κB signaling and necroptosis. Though both receptors are ubiquitously expressed, their relative participation in TRAIL-induced signaling is still largely unknown. To analyze TRAIL receptor-specific signaling, we prepared Strep-tagged, trimerized variants of recombinant human TRAIL with high affinity for either DR4 or DR5 receptor. Using these receptor-specific ligands, we examined the contribution of individual pro-apoptotic receptors to TRAIL-induced signaling pathways. We found that in TRAIL-resistant colorectal HT-29 cells but not in pancreatic PANC-1 cancer cells, DISC formation and initial caspase-8 processing proceeds comparably via both DR4- and DR5-activated signaling. TRAIL-induced apoptosis, enhanced by the inhibitor of the Bcl-2 family ABT-737, or by the translation inhibitor homoharringtonine, proceeded in both cell lines predominantly via the DR5 receptor. ShRNA-mediated downregulation of DR4 or DR5 receptors in HT-29 cells also pointed to a stronger contribution of DR5 in TRAIL-induced apoptosis. In contrast to apoptosis, necroptotic signaling was activated similarly by both DR4- or DR5-specific ligands. Activation of auxiliary signaling pathways involving NF-κB or stress kinases proceeded under apoptotic conditions mainly in a DR5-dependent manner, while these signaling pathways were during necroptosis similarly activated by either of these ligands. Our study provides the first systematic insight into DR4 ?/DR5-specific signaling in colorectal and pancreatic cancer cells.