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1.
G3 (Bethesda) ; 13(5)2023 05 02.
Article in English | MEDLINE | ID: mdl-36911920

ABSTRACT

Numerous mutants of the nematode Caenorhabditis elegans with surface abnormalities have been isolated by utilizing their resistance to a variety of bacterial pathogens (Microbacterium nematophilum, Yersinia pseudotuberculosis, and 2 Leucobacter strains), all of which are able to cause disease or death when worms are grown on bacterial lawns containing these pathogens. Previous work led to the identification of 9 srf or bus genes; here, we report molecular identification and characterization of a further 10 surface-affecting genes. Three of these were found to encode factors implicated in glycosylation (srf-2, bus-5, and bus-22), like several of those previously reported; srf-2 belongs to the GT92 family of putative galactosyltransferases, and bus-5 is homologous to human dTDP-D-glucose 4,6-dehydratase, which is implicated in Catel-Manzke syndrome. Other genes encoded proteins with sequence similarity to phosphatidylinositol phosphatases (bus-6), Patched-related receptors (ptr-15/bus-13), steroid dehydrogenases (dhs-5/bus-21), or glypiation factors (bus-24). Three genes appeared to be nematode-specific (srf-5, bus-10, and bus-28). Many mutants exhibited cuticle fragility as revealed by bleach and detergent sensitivity; this fragility was correlated with increased drug sensitivity, as well as with abnormal skiddy locomotion. Most of the genes examined were found to be expressed in epidermal seam cells, which appear to be important for synthesizing nematode surface coat. The results reveal the genetic and biochemical complexity of this critical surface layer, and provide new tools for its analysis.


Subject(s)
Caenorhabditis elegans Proteins , Animals , Humans , Caenorhabditis elegans Proteins/genetics , Mutation , Caenorhabditis elegans/genetics , Bacteria/metabolism , Glycosylation
2.
Sci Adv ; 8(19): eabi6690, 2022 May 13.
Article in English | MEDLINE | ID: mdl-35559683

ABSTRACT

Scaling the number of qubits while maintaining high-fidelity quantum gates remains a key challenge for quantum computing. Presently, superconducting quantum processors with >50 qubits are actively available. For these systems, fixed-frequency transmons are attractive because of their long coherence and noise immunity. However, scaling fixed-frequency architectures proves challenging because of precise relative frequency requirements. Here, we use laser annealing to selectively tune transmon qubits into desired frequency patterns. Statistics over hundreds of annealed qubits demonstrate an empirical tuning precision of 18.5 MHz, with no measurable impact on qubit coherence. We quantify gate error statistics on a tuned 65-qubit processor, with median two-qubit gate fidelity of 98.7%. Baseline tuning statistics yield a frequency-equivalent resistance precision of 4.7 MHz, sufficient for high-yield scaling beyond 103 qubit levels. Moving forward, we anticipate selective laser annealing to play a central role in scaling fixed-frequency architectures.

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