{'fraction_non_alphanumeric': 0.01958955223880597, 'fraction_numerical': 0.0046641791044776115, 'mean_word_length': 5.967532467532467, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Two Functionally Redundant Sliding Modules Drive Chromosome Segregation

Proper chromosome segregation into two future daughter cells requires the mitotic spindle to elongate in anaphase. Yet, the molecular mechanism that drives spindle elongation in human cells is unknown. Using combined depletion and inactivation assays together with CRISPR technology to explore redundancy between multiple targets, we discovered that the force-generating mechanism of spindle elongation consists of the PRC1-dependent motor KIF4A/kinesin-4 together with EG5/kinesin-5. Disruption of both motors leads to total failure of chromosome segregation due to blocked spindle elongation, despite poleward chromosome motion. Tubulin photoactivation and super-resolution microscopy show that perturbation of both proteins impairs midzone microtubule sliding without affecting microtubule stability. Thus, two mechanistically distinct sliding modules, one based on a self-sustained and the other on a crosslinker-assisted motor, power the mechanism that drives spindle elongation in human cells.