Press-room / Digest
Antibiotic from the bear's mouth
Scientists from the Laboratory of biocatalysis developed a new microfluidics-based ultrahigh-throughput technology for the “deep functional profiling” of microbial communities and used it to search for bacteria producing new antibiotics in the microbiome of the Siberian bear's oral cavity. This methodology allowed them not only to find the antibiotic amicoumacin, elucidating the mechanisms of its biosynthesis and self-resistance, but also to investigate the spectrum of its activity at the level of various bacterial communities. The results published in PNAS will find numerous applications in the field of antibiotic discovery and will help to solve the problem of antibiotic resistance.
Spider venom may help to stop neuronal death
Venoms of spiders and wasps contain acylpolyamines that act as high-affinity blockers of ionotropic receptors for glutamate, the main excitatory neurotransmitter in the human central nervous system (CNS). The first representative of acylpolyamines, argiopin from the venom of the orb-weaver spider Argiope lobata, was discovered in 1986 by Eugene Grishin’s team at IBCh RAS. Here, an international team of scientists, including a researcher from IBCh RAS, has used cryo-electron microscopy (cryo-EM) to determine the first atomic structure of an argiopin-glutamate receptor complex.
Genetically encoded fluorescent pH probe for precise monitoring of cellular biochemistry
One of the directions of the Molecular Technologies Laboratory is the development of new tools for bioimaging and optogenetics. Yulia Ermakova, Vsevolod Belousov and other lab members, in an article in Chemical Communications, describe a new member of SypHer family of genetically encoded pH indicators, SypHer3s.
Spider venom will cure from paralysis
Scientists from IBCh RAS together with foreign colleagues discovered that a toxin from the venom of the spider Heriaeus melloteei may serve as a hit in drug discovery for hypokalemic periodic paralysis type 2. The disease is caused by mutations in the gene encoding voltage-gated sodium channels NaV1.4, characteristic of skeletal muscles. As a result of the mutations, these channels conduct aberrant currents, the muscles are unable to respond to the signals of the nervous system, and weakness develops followed by paralysis. Until now, there is no reliable medication for all cases of this disease.