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Lytic polysaccharide mono-oxygenases oxidatively cleave the glycosidic chain on the crystalline surface of cellulose or chitin to create an entry point for hydrolytic cellulases or chitinases. The discovery of a new family of lytic polysaccharide mono-oxygenases expands the possibilities for the use of these enzymes to accelerate biomass degradation.
Crystal structures of QueE, a radical SAM enzyme that converts the purine base of GTP into a deazapurine found in natural products and tRNA, explain how the enzyme functions with a trimmed-down radical SAM enzyme fold and rationalizes its unusual Mg2+ dependency.
Use of a domain of unknown function as the input for bioinformatic searching reveals a new Cu-dependent family of chitinases, assigned as CAZy group AA11, that diverge in sequence but share structural homology with the existing AA9 and AA10 families.
Phenotypic screening for serine hydrolase inhibitors capable of modulating lipid storage coupled with target deconvolution identifies carboxylesterase 3 as having a role in regulating adipocyte function, with enzyme inhibition causing positive outcomes in mouse models of obesity and diabetes.
Altered glycosylation of cancer cells confers phenotypic changes that promote spread and evasion of immune responses. A new method for engineering cell surface glycans is providing insights into these mechanisms.
Iron is essential for biological systems but can also damage or kill cells, leading to a variety of disease states. A review of mechanisms leading to Fe- and ROS-dependent cell death highlights the vast array of open questions in this complex field.
A screen for compounds that promote ES cell differentiation into pancreatic β cells identified a VMAT2- and monoamine-dependent suppression mechanism of pancreatic β-cell differentiation. VMAT2 inhibitors potentiated differentiation from Pdx1-positive pancreatic progenitor cells into Ngn3-positive endocrine precursors, and then into β cells with increased insulin production.
In the ubiquitin-proteasome system, E2 enzymes such as Cdc34A mediate the transfer of ubiquitin to protein substrates, which are thus marked for proteasomal degradation or other fates. New structural data reveal that the small-molecule inhibitor CC0651 impairs Cdc34A activity by stabilizing the normally transient Cdc34A–ubiquitin complex.
In synthetic biology designs, circuit components can generally move within the cell, meaning that functional cross-talk can cause faulty wiring. Genome mining, synthetic promoter construction and cross-reactivity screening now identify 20 orthogonal TetR repressor-promoter pairs for use in complex applications.
TR3 is an orphan nuclear receptor with roles in apoptosis. A TR3-binding compound induces mitochondrial translocation of TR3 and autophagy via the Nix–Toms–ANT1/VDAC1 pathway, providing a mechanism for cell death in melanoma cells that are resistant to spontaneous and drug-induced apoptosis.
Substrate binding to the multidrug exporter LmrP from Lactococcus lactis catalyzes proton entrance by stabilizing an outward-open conformation. Transitions between conformational states are dictated by proton passage down the transmembrane helical bundle.
Certain adenosine residues within mammalian RNAs undergo reversible N6 methylation. Two methyltransferase enzymes, METTL3 and METTL14, as well as the splicing factor WTAP are identified as core components of the multiprotein complex that deposits RNA N6-methyladenosine (m6A) in nuclear RNAs.
