Mikhail A. Khodorkovskii

This paper introduces an active learning method to discover PAMs for uncharacterized CRISPR-Cas9 orthologs without sequencing, reducing data requirements and validating it on known and novel Cas9 variants.

The paper shows PARP1 binding weakens nucleosome core contacts using optical tweezers.

This study characterizes SuCas9, a compact Cas9 ortholog from Streptococcus uberis, showing it can cleave DNA in vitro and function in human cells with a novel PAM sequence.

This study shows that plasmid copy number affects the expression dynamics and phage resistance of the CfrBI R-M system, with medium-copy plasmids providing the highest resistance.

This study investigates the FtsZ protein in Mycoplasma gallisepticum, showing it localizes polarly rather than mid-cell and can polymerize, supporting its role in cell division despite differences from other homologs.

This study identifies a single DNA binding site in DprA dimer that facilitates RecA filament nucleation on short ssDNA.

This study uses optical tweezers to investigate RecN's interactions with ssDNA and dsDNA, revealing its predominant ssDNA binding and weak dsDNA binding that forms DNA loop-like structures.

The paper describes the EPI vesicle, a structure used by the phiKZ phage to transport viral DNA during early infection, protecting it from bacterial nucleases.

This study uses fluorescence microscopy and single-molecule techniques to investigate RecN's localization and DNA-binding properties in Escherichia coli.

The paper describes modifications to the CRISPR-Cas12d system, identifies catalytically inactive variants, and demonstrates their high specificity using single-molecule techniques.

This study investigates the localization dynamics of two phage-encoded RNA polymerases during phiKZ infection, showing vRNAP is injected and excluded from the phage nucleus while nvRNAP is synthesized and localized within the nucleus.

This study investigates how RecX regulates RecA-ssDNA filament conformational states in E. coli, revealing that RecX binds the inactive state and inhibits transition to the active state.