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Excitation of single molecules with electrons tunneling between a sharp metallic tip of a scanning tunneling microscope and a metal surface is one way to study and control dynamics of molecules on surfaces. Electron tunneling induced dynamics may lead to hopping, rotation, molecular switching, or chemical reactions. Molecular motors that convert rotation of subgroups into lateral movement on a surface can in principle also be driven by tunneling electrons. For such surface-bound motor molecules the efficiency of motor action with respect to electron dose is still not known. Here, the response of a molecular motor containing two rotor units in the form of overcrowded alkene groups to inelastic electron tunneling has been examined on a Cu(111) surface in ultrahigh vacuum at 5 K. Upon vibrational excitation, switching between different molecular conformations is observed, including conversion of enantiomeric states of chiral conformations. Tunneling at energies in the range of electronic excitations causes activation of motor action and movement across the surface. The expected unidirectional rotation of the two rotor units causes forward movements but with a low degree of translational directionality.

Pyroptosis is an inflammatory form of cell death induced upon recognition of invading microbes. During an infection, pyroptosis is enhanced in interferon-gamma-exposed cells via the actions of members of the guanylate-binding protein (GBP) family. GBPs promote caspase-4 (CASP4) activation by enhancing its interactions with lipopolysaccharide (LPS), a component of the outer envelope of Gram-negative bacteria. Once activated, CASP4 promotes the formation of noncanonical inflammasomes, signaling platforms that mediate pyroptosis. To establish an infection, intracellular bacterial pathogens, like Shigella species, inhibit pyroptosis. The pathogenesis of Shigella is dependent on its type III secretion system, which injects ~30 effector proteins into host cells. Upon entry into host cells, Shigella are encapsulated by GBP1, followed by GBP2, GBP3, GBP4, and in some cases, CASP4. It has been proposed that the recruitment of CASP4 to bacteria leads to its activation. Here, we demonstrate that two Shigella effectors, OspC3 and IpaH9.8, cooperate to inhibit CASP4-mediated pyroptosis. We show that in the absence of OspC3, an inhibitor of CASP4, IpaH9.8 inhibits pyroptosis via its known degradation of GBPs. We find that, while some LPS is present within the host cell cytosol of epithelial cells infected with wild-type Shigella, in the absence of IpaH9.8, increased amounts are shed in a GBP1-dependent manner. Furthermore, we find that additional IpaH9.8 targets, likely GBPs, promote CASP4 activation, even in the absence of GBP1. These observations suggest that by boosting LPS release, GBP1 provides CASP4-enhanced access to cytosolic LPS, thus promoting host cell death via pyroptosis.

Pyroptosis is an inflammatory form of cell death induced upon the recognition of invading microbes. During an infection, pyroptosis is enhanced in interferon-gamma (IFNγ) exposed cells due to the actions of members of the guanylate binding protein (GBP) family. GBPs promote activation of caspase-4 (CASP4) by enhancing its interactions with lipopolysaccharide (LPS), a component of the outer envelope of Gram-negative bacteria. Once activated, CASP4 promotes the formation of non-canonical inflammasomes, signaling platforms that mediate pyroptosis. To establish an infection, intracellular bacterial pathogens, likeShigellaspecies, inhibit pyroptosis. The pathogenesis ofShigellais dependent on its type III secretion system, which injects ~30 effector proteins into host cells. Upon entry into host cells,Shigellaare encapsulated by GBP1, followed by GBP2, GBP3, GBP4, and in some cases, CASP4. It has been suggested that the recruitment of CASP4 to bacteria leads to its activation. Here, we demonstrate that twoShigellaeffectors, OspC3 and IpaH9.8, cooperate to inhibit CASP4-mediated pyroptosis. We show that in the absence of OspC3, an inhibitor of CASP4, IpaH9.8 inhibits pyroptosis via its known degradation of GBPs. We find that, while some LPS is present within the host cell cytosol of epithelial cells infected with wild typeShigella, in the absence of IpaH9.8, increased amounts are shed in a GBP1-dependent manner. Furthermore, that additional IpaH9.8 targets, likely GBPs, promote CASP4 activation, even in the absence of GBP1. These observations suggest that by promoting LPS release, GBP1 provides CASP4 access to LPS, thus promoting host cell death via pyroptosis.Significance StatementNon-canonical inflammasomes mediate the death of intestinal epithelial cells in response to invading Gram-negative bacterial pathogens. CASP4 is activated upon binding to LPS. Recent studies have suggested that GBP1 recruits and enables the activation of CASP4 on the surface of intracytosolic bacteria. This has led to the proposal that non-canonical inflammasomes assemble on the bacterial surface due to GBP1-mediated access of CASP4 to the membrane-embedded lipid A component of LPS. Here, we show that by targeting the degradation of GBPs,ShigellaIpaH9.8 limits the release of LPS from intracellularShigellainto the host cell cytosol in a GBP1-dependent manner. Furthermore, we find evidence to suggest that in the absence of GBP1, other members of the GBP family promote CASP4 activation.

The thermally induced cyclodehydrofluorization of iron tetrakis(pentafluorophenyl)porphyrin proceeded highly stereoselectively to give a prochiral product on a gold surface in an ultrahigh vacuum, whereas dehydrocyclization of the respective iron tetrakisphenylporphyrin did not show such selectivity. Stereoselectivity was predominantly observed for closely packed layers, which is an indication of intermolecular cooperativity and steric constraints induced by adjacent species. Density functional theory identified intermolecular packing constraints as the origin of such selectivity during the reaction. Scanning tunneling microscopy revealed the formation of an enantiomerically pure two-dimensional self-assembly as a conglomerate of mirror domains. On-surface two-dimensional topochemistry, as reported herein, may open new routes for stereoselective synthesis.

Resolution of enantiomers of chiral compounds via crystallization is the dominant method in chemical industry, but chiral recognition at the molecular level during this process is still poorly understood. Using single metal surfaces in ultrahigh vacuum as model system, the enantio-related transition from the monolayer structure into a double layer of the racemic mixture of heptahelicene has been studied with scanning tunneling microscopy. Submolecular resolution reveals enantiopure second layers on Ag(111) and almost enantiopure second layers on Au(111). In analogy to previous results on Cu(111), it is concluded that transition from the 2D first layer racemate into a layered racemate occurs.

The chiral self‐assembly of trispentahelicene propellers on a gold surface has been investigated in ultrahigh vacuum by means of scanning tunneling microscopy and time‐of‐flight secondary ion mass spectrometry. The trispentahelicene propellers aggregate into mirror domains with an enantiomeric ratio of 2 : 1. Thermally induced cyclodehydrogenation leads to planarization into nanographenes, which self‐assemble into closed‐packed layers with two different azimuths. Further treatment induces in part dimerization and trimerization by intermolecular cyclodehydrogenation., From helical to planar: Molecular propellers built up by three pentahelicene subunits self‐assemble on a gold surface into enantiomerically unbalanced two‐dimensional crystal domains. Upon thermal treatment of the close‐packed monolayer, intramolecular cyclodehydrogenation into planar nanographenes occurs. Further thermal treatment leads in part to fusion into larger graphene flakes of up to four nanographene units by intermolecular cyclodehydrogenation.

The modification of metal electrode surfaces with functional organic molecules is an important part of organic electronics. The interaction of the buckminsterfullerene fragment molecule pentaindenocorannulene with a Cu(100) surface is studied by scanning tunneling microscopy, dispersion-enabled density functional theory, and force field calculations. Experimental and theoretical methods suggest that two adjacent indeno groups become oriented parallel to the surface upon adsorption under mild distortion of the molecular frame. The binding mechanism between molecule and surface is dominated by strong electrostatic interaction owing to Pauli repulsion. Two-dimensional aggregation at room temperature leads to a single lattice structure in which all molecules are oriented unidirectionally. Their relative arrangement in the lattice suggests noncovalent intermolecular interaction through C-H⋅⋅⋅π bonding.

The growth of carbon layers, defective graphene, and graphene by deposition of polycyclic aromatic hydrocarbons (PAHs) on Cu(111) is studied by scanning tunneling microscopy and X-ray photoelectron spectroscopy. Two different PAHs are used as starting materials: the buckybowl pentaindenocorannulene (PIC) which contains pentagonal rings and planar coronene (CR). For both precursors, with increasing sample temperature during deposition, porous carbon aggregates (350 °C), dense carbon layers (400-450 °C), disordered defective graphene (500 °C-550 °C), and extended graphene (≥600 °C) are obtained. No significant differences for defective graphene grown from PIC and CR are observed. C 1s X-ray photoelectron spectra of PIC and CR derived samples grown at 350-550 °C exhibit a characteristic C-Cu low binding energy component. Preparation at ≥600 °C eliminates this C-Cu species and only C-C bonded carbon remains.