Search bioRxiv⌕ Search

bioRxiv · 10.1101/838433

Proposed mechanism of kinesin backstepping

Abstract

Kinesin-1 is an ATP-driven molecular motor that transports cellular cargo along microtubules. At low loads, kinesin-1 almost always steps forwards, towards microtubule plus ends, but at higher loads, it can also step backwards. Backsteps are usually 8 nm, but can be larger. These larger backwards events of 16 nm, 24 nm or more are thought to be slips rather than steps, because they are too fast to consist of multiple, tightly-coupled 8 nm steps. Here we propose that not just these larger backsteps, but all kinesin-1 backsteps, are slips. We show firstly that kinesin waits before forward steps for less time than before backsteps and detachments; secondly that kinesin waits for the same amount of time before backsteps and detachments and thirdly that by varying the microtubule type we can change the ratio of backsteps to detachments, without affecting forward stepping. Our findings indicate that backsteps and detachments originate from the same state and that this state arises later in the mechanochemical cycle than the state that gives rise to forward steps. To explain our data, we propose that in each cycle of ATP turnover, forward kinesin steps can only occur before Pi release, whilst backslips and detachments can only occur after Pi release. In the scheme we propose, Pi release gates access to a weak binding K.ADP-K.ADP state that can slip back along the microtubule, re-engage, release ADP and try again to take an ATP-driven forward step. We predict that this rescued detachment pathway is key to maintaining kinesin processivity under load. Significance statementKinesin-1 molecular motors are ATP-driven walking machines that typically step forward, towards microtubule plus ends. But they can also step backwards, especially at high load. Backsteps are currently thought to occur by directional reversal of forwards walking. To the contrary, we propose here that kinesin backsteps are not steps, but slips. We show that backwards translocations originate from a different and later state in the kinesin mechanism than the state that generates forward steps. To explain this, we propose that following ATP binding, kinesin molecules that fail to step forward within a load-dependent time window convert to a state that can slip back, rebind to the microtubule, and try again to step forward.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Toleikis, A., Carter, N. J., Cross, R. A.. 2019-11-12. Proposed mechanism of kinesin backstepping. https://doi.org/10.1101/838433

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Design of colipids with controlled lateral distance of head group moieties for targeting strategies in the field of lipid-based nanoparticles

Lipid nanoparticles and liposomes are nanoparticle drug formulations which are firmly established in clinics. In order to expand their application and improve efficacy, surface modifications can be a key strategy, especially for cell specific targeting. Targeting can be achieved by integrating ligand functionalized lipids or lipidoids on the nanoparticle surface. In this case, not solely the targeting ligand itself, but also the structure of the whole targeting lipid/lipidoid can affect the interaction of the targeting ligand with the binding motive on cells. Especially, distal spacer structures between lipid anchor and ligand unit, often composed of polyethylene glycol chains, provide a certain distance of the ligand from the nanoparticle surface. A concept which is currently neglected is the control of the lateral distance between ligand structures on the nanoparticle. Herein we investigated the possibility to design lipidoids with a lateral spacer composed of polyethylene glycol units. We synthesized and characterized different lipidoids which provide a primary amine in the head group for possible ligand coupling. In our model lipidoids the head groups were functionalized with a paramagnetic probe to apply electron paramagnetic resonance (EPR) methods for the characterization of the lipidoid interaction with model nanoparticles, in our case liposomes. Continuous wave EPR was used to study the efficiency of the novel lipidoids to integrate into lipid bilayers of model liposomes, which was shown to depend on lipidoid structure and liposome composition. Furthermore, using double electron-electron resonance (DEER), we observed lipidoid conformational changes occurring upon integration into liposomes.

biophysics↗

Binding mechanisms of therapeutic antibodies to human claudin-18.2

Claudin-18.2 (CLDN18.2) is a tight junction component with highly restricted expression in the paracellular space of nonmalignant gastric epithelial cells. It becomes accessible on tumor cell surface during malignant transformation, making CLDN18.2 an attractive target for targeted therapies against gastric cancer. Recently, zolbetuximab has become the first FDA-approved monoclonal antibody that targets CLDN18.2 in advanced gastric cancer, and others like osemitamab have entered phase 3 clinical trials. However, the high-resolution structure of CLDN18.2 is lacking, and how CLDN18.2 is recognized by therapeutic antibodies remains undefined. Here, we report cryo-EM structures of human claudin-18.2 (hCLDN18.2) in complex with the Fab fragments of zolbetuximab and osemitamab, revealing the structure of hCLDN18.2 and its binding mechanism to the therapeutic antibodies. Further analyses reveal that three residues in the first extracellular loop of hCLDN18.2 that are different from human claudin-18.1 (hCLDN18.1) play a critical role in antibody binding. Our data elucidate the structural basis for selective binding of therapeutic antibodies to hCLDN18.2, which should aid rational design of next-generation immunotherapies targeting hCLDN18.2.

biophysics↗

Structural relationships between the SLC12 cotransporter C-terminal domain, universal stress proteins and adenylating enzymes

Several SLC12 cotransporters bind ATP in a cytoplasmic C-terminal domain (CTD). We analysed 16,192 CTD-containing SLC12 sequences and compared 42,845 representative structures to examine the relationship between this nucleotide site, universal stress proteins (USPs) and adenylating enzymes. In phosphorylated NKCC1, D891 and D927 lie near the ATP phosphate chain, while R801 and K889 form a basic phosphate-binding clamp. NKCC1 retains this arrangement, whereas KCC paralogs replace or lose several corresponding groups. In structural comparisons with USP and adenylating-enzyme references, both CTD lobes score between universal stress proteins and EC-annotated domains, and the two lobes form separate lineages that include bacterial transporters. Lobe-specific and nucleotide-frame comparisons place ATP in the corresponding structural region used for -phosphate chemistry by catalytic members of this fold. Published work on UspG provides a precedent for protein-bound AMP in a natural USP. In the examined SLC12 structures and USP models, candidate protein hydroxyls lack an in-line geometry for attack at ATP P. Protein adenylation would require a change in protein or nucleotide geometry, or a different acceptor. These results define a structural basis for testing conditional protein adenylation at SLC12 nucleotide sites. The required evidence is a covalent protein-AMP adduct, identification of its acceptor and measurement of the expected pyrophosphate coproduct, with soluble nucleotide analysis to distinguish accompanying ATP reactions.

biophysics↗