We present the complete genome sequence of uropathogenic Escherichia coli, strain CFT073. A three-way genome comparison of the CFT073, enterohemorrhagic E. coli EDL933, and laboratory strain MG1655 reveals that, amazingly, only 39.2% of their combined (nonredundant) set of proteins actually are common to all three strains. The pathogen genomes are as different from each other as each pathogen is from the benign strain. The difference in disease potential between O157:H7 and CFT073 is reflected in the absence of genes for type III secretion system or phage-and plasmid-encoded toxins found in some classes of diarrheagenic E. coli. The CFT073 genome is particularly rich in genes that encode potential fimbrial adhesins, autotransporters, iron-sequestration systems, and phase-switch recombinases. Striking differences exist between the large pathogenicity islands of CFT073 and two other well-studied uropathogenic E. coli strains, J96 and 536. Comparisons indicate that extraintestinal pathogenic E. coli arose independently from multiple clonal lineages. The different E. coli pathotypes have maintained a remarkable synteny of common, vertically evolved genes, whereas many islands interrupting this common backbone have been acquired by different horizontal transfer events in each strain.

Despite decades of research, general purpose inhand manipulation remains one of the unsolved challenges of robotics. One of the contributing factors that limit current robotic manipulation systems is the difficulty of precisely sensing contact forces -sensing and reasoning about contact forces are crucial to accurately control interactions with the environment. As a step towards enabling better robotic manipulation, we introduce DIGIT, an inexpensive, compact, and high-resolution tactile sensor geared towards in-hand manipulation. DIGIT improves upon past vision-based tactile sensors by miniaturizing the form factor to be mountable on multi-fingered hands, and by providing several design improvements that result in an easier, more repeatable manufacturing process, and enhanced reliability. We demonstrate the capabilities of the DIGIT sensor by training deep neural network model-based controllers to manipulate glass marbles in-hand with a multi-finger robotic hand. To provide the robotic community access to reliable and low-cost tactile sensors, we open-source the DIGIT design at www.digit.ml.

SummaryThe nematode Caenorhabditis elegans has been much studied as a host for microbial infection. Some pathogens can infect its intestine [1, 2], while others attack via its external surface [1, 3–6]. Cultures of Caenorhabditis isolated from natural environments have yielded new nematode pathogens, such as microsporidia and viruses [7, 8]. We report here a novel mechanism for bacterial attack on worms, discovered during investigation of a diseased and coinfected natural isolate of Caenorhabditis from Cape Verde. Two related coryneform pathogens (genus Leucobacter) were obtained from this isolate, which had complementary effects on C. elegans and related nematodes. One pathogen, Verde1, was able to cause swimming worms to stick together irreversibly by their tails, leading to the rapid formation of aggregated “worm-stars.” Adult worms trapped in these aggregates were immobilized and subsequently died, with concomitant growth of bacteria. Trapped larval worms were sometimes able to escape from worm-stars by undergoing autotomy, separating their bodies into two parts. The other pathogen, Verde2, killed worms after rectal invasion, in a more virulent version of a previously studied infection [6]. Resistance to killing by Verde2, by means of alterations in host surface glycosylation, resulted in hypersensitivity to Verde1, revealing a trade-off in bacterial susceptibility. Conversely, a sublethal surface infection of worms with Verde1 conferred partial protection against Verde2. The formation of worm-stars by Verde1 occurred only when worms were swimming in liquid but provides a striking example of asymmetric warfare as well as a bacterial equivalent to the trapping strategies used by nematophagous fungi [4].

The surface of the nematode Caenorhabditis elegans is poorly understood but critical for its interactions with the environment and with pathogens. We show here that six genes (bus-2, bus-4, and bus-12, together with the previously cloned srf-3, bus-8, and bus-17) encode proteins predicted to act in surface glycosylation, thereby affecting disease susceptibility, locomotory competence, and sexual recognition. Mutations in all six genes cause resistance to the bacterial pathogen Microbacterium nematophilum, and most of these mutations also affect bacterial adhesion and biofilm formation by Yersinia species, demonstrating that both infection and biofilm formation depend on interaction with complex surface carbohydrates. A new bacterial interaction, involving locomotory inhibition by a strain of Bacillus pumilus, reveals diversity in the surface properties of these mutants. Another biological property-contact recognition of hermaphrodites by males during mating-was also found to be impaired in mutants of all six genes. An important common feature is that all are expressed most strongly in seam cells, rather than in the main hypodermal syncytium, indicating that seam cells play the major role in secreting surface coat and consequently in determining environmental interactions. To test for possible redundancies in gene action, the 15 double mutants for this set of genes were constructed and examined, but no synthetic phenotypes were observed. Comparison of the six genes shows that each has distinctive properties, suggesting that they do not act in a linear pathway.