The potential role of public gardens as sentinels of plant invasion

Public gardens can help prevent detrimental effects of plant invasions by collecting and sharing data on taxa spreading from cultivation early in the invasion process, thereby acting as sentinels of plant invasion. Existing initiatives have called for public gardens to adopt measures preventing plant invasion, but it is unclear what actions individual gardens are implementing, as there is no formal mechanism for communicating their progress. This study used internal lists of escaping taxa from seven public gardens in the Midwestern United States and Canada to demonstrate how public gardens can collectively contribute data that is critical to assessing potential invasiveness. It also reveals methodological differences in how gardens develop their lists of escaping plants, leading to recommendations for standardization. Data pooled across gardens yielded 769 species spreading from cultivation at one or more gardens. Eight woody species were listed by all gardens despite not consistently being recognized as invasive by states and provinces containing the gardens; some species recorded by multiple gardens did not appear on any invasive lists. While it may be premature to call taxa escaping from cultivation at a few public gardens “invasive” or even “potentially invasive”, these plants should be monitored and evaluated with this information shared to facilitate stronger conclusions about risk. Thus, public gardens have a unique expertise in assisting invasive plant efforts as sentinels, particularly if challenges related to methodological inconsistencies and data sharing are suitably addressed, which is herein recommended through the adoption of a set of standardized guidelines.

     

Natural variability of minimotifs in 1092 people indicates that minimotifs are targets of evolution

Since the function of a short contiguous peptide minimotif can be introduced or eliminated by a single point mutation, these functional elements may be a source of human variation and a target of selection. We analyzed the variability of ∼300 000 minimotifs in 1092 human genomes from the 1000 Genomes Project. Most minimotifs have been purified by selection, with a 94% invariance, which supports important functional roles for minimotifs. Minimotifs are generally under negative selection, possessing high genomic evolutionary rate profiling (GERP) and sitewise likelihood-ratio (SLR) scores. Some are subject to neutral drift or positive selection, similar to coding regions. Most SNPs in minimotif were common variants, but with minor allele frequencies generally <10%. This was supported by low substation rates and few newly derived minimotifs. Several minimotif alleles showed different intercontinental and regional geographic distributions, strongly suggesting a role for minimotifs in adaptive evolution. We also note that 4% of PTM minimotif sites in histone tails were common variants, which has the potential to differentially affect DNA packaging among individuals. In conclusion, minimotifs are a source of functional genetic variation in the human population; thus, they are likely to be an important target of selection and evolution.     

Nanomolar affinity,iminosugar-based chemical probes for specific labeling of lysosomal glucocerebrosidase

Three different photoprobes were synthesized to label β-glucosidases; one probe was based on glucose, two probes on the iminosugar deoxynojirimycin. The affinity of the probes for three different β-glucosidases was determined. Furthermore, their labeling efficiencies, binding specificities through competition with deoxynojirimycin, and binding specificities in the presence of cell lysate, were evaluated. Especially one showed very high affinity towards non-lysosomal glucoceramidase (IC₅₀ = 20 nM).     

Multiple cholesterol recognition/interaction amino acid consensus (CRAC) motifs in cytosolic C tail of Slo1 subunit determine cholesterol sensitivity of Ca2+- and voltage-gated K+ (BK) channels

Large conductance, Ca(2+)- and voltage-gated K(+) (BK) channel proteins are ubiquitously expressed in cell membranes and control a wide variety of biological processes. Membrane cholesterol regulates the activity of membrane-associated proteins, including BK channels. Cholesterol modulation of BK channels alters action potential firing, colonic ion transport, smooth muscle contractility, endothelial function, and the channel alcohol response. The structural bases underlying cholesterol-BK channel interaction are unknown. Such interaction is determined by strict chemical requirements for the sterol molecule, suggesting cholesterol recognition by a protein surface. Here, we demonstrate that cholesterol action on BK channel-forming Cbv1 proteins is mediated by their cytosolic C tail domain, where we identified seven cholesterol recognition/interaction amino acid consensus motifs (CRAC4 to 10), a distinct feature of BK proteins. Cholesterol sensitivity is provided by the membrane-adjacent CRAC4, where Val-444, Tyr-450, and Lys-453 are required for cholesterol sensing, with hydrogen bonding and hydrophobic interactions participating in cholesterol location and recognition. However, cumulative truncations or Tyr-to-Phe substitutions in CRAC5 to 10 progressively blunt cholesterol sensitivity, documenting involvement of multiple CRACs in cholesterol-BK channel interaction. In conclusion, our study provides for the first time the structural bases of BK channel cholesterol sensitivity; the presence of membrane-adjacent CRAC4 and the long cytosolic C tail domain with several other CRAC motifs, which are not found in other members of the TM6 superfamily of ion channels, very likely explains the unique cholesterol sensitivity of BK channels.     

Enhancing membrane disruption by targeting and multivalent presentation of antimicrobial peptides

In order to enhance the membrane disruption of antimicrobial peptides both targeting and multivalent presentation approaches were explored. The antimicrobial peptides anoplin and temporin L were conjugated via click chemistry to vancomycin and to di- and tetravalent dendrimers. The vancomycin unit led to enhanced membrane disruption of large unilamellar vesicles (LUVs) displaying the vancomycin target lipid II, but only for temporin L and not for anoplin. The multivalent presentation led to enhanced LUV membrane disruption in the case of anoplin but not for temporin L.