| Popis: |
Autophagy is an evolutionarily conserved degradation mechanism of misfolded proteins and damaged organelles which helps maintain cellular homeostasis. Besides its canonical function, proteins of the autophagy pathway also participate in other cellular processes including chromosome congression. Here, we perform a comprehensive screen of autophagy mutants in yeast and found that cells lacking an autophagy-related protein Atg11 have poor mitotic stability of linear and circular chromosomes. atg11Δ cells grow slowly at 37°C and accumulate at metaphase with aberrant astral microtubules (aMTs) along with mispositioned and misaligned spindles. Deletion of the spindle positioning checkpoint (SPOC) factor Bub2, but not the spindle assembly checkpoint (SAC) component Mad2, could improve the growth of the atg11Δ cells. Strikingly, the spindle pole body (SPB) localization pattern of an SPB component Spc72 is found to be randomized in atg11Δ cells resulting in inverted SPB inheritance. Atg11 is transiently localized to SPBs and interacts both physically and genetically with Spc72. Taken together, our study uncovers a moonlighting function of Atg11 participating between spatially separated processes, the cell cycle and autophagy, essential for proper spindle positioning and asymmetric SPB inheritance. Our findings, therefore, highlight one of the many failsafe mechanisms likely in place to ensure asymmetric cell division. |
