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Two studies reveal a conserved, noncatalytic role for Topo II’s C-terminal domain in recruiting the checkpoint kinase Aurora B.

People & Ideas

Kraft’s work focuses on the mechanisms that regulate autophagy in response to nutrient availability.



In Special Collection: Mitochondrial Biology Reviews


Encarnação et al. show that Rab3a, together with its newly identified effector NMHC IIA, mediates the positioning of peripheral lysosomes in nonsecretory cells, thereby promoting lysosome exocytosis and plasma membrane repair.

Using optogenetics to obtain spatiotemporal control of RhoA activation, Wagner and Glotzer show that local RhoA activation is sufficient to induce cytokinetic furrowing. Furrows can be induced at both the cell equator and cell poles during various stages of mitosis, and cell rounding allows active RhoA to induce furrows in interphase.


The C-terminal domain (CTD) of Topo II is dispensable for its catalytic activity yet essential for Topo II function in chromosome segregation during mitosis. Here, Edgerton et al. resolve the role of the Topo II CTD during mitosis in yeast, showing that it functions noncatalytically via the Haspin-H3 T3-Phos pathway to recruit Ipl1/Aurora B to mitotic inner centromeres.

Yoshida et al. show that mitotic SUMOylation of TOP2A C-terminal domain promotes its association with phosphorylated Haspin kinase through Haspin’s SUMO-interacting motifs to regulate recruitment of Aurora B kinase at mitotic centromeres.

Differentiation induces loss of centrosomal microtubule organizing activity in many cell types, though the underlying mechanisms are poorly understood. Using the epidermis, Muroyama et al. show that cell cycle exit causes loss of a Nedd1–γ-tubulin complex, which is required for anchoring microtubules at the centrosome. This defines a novel function for γ-tubulin complexes in microtubule anchoring at the centrosome.

Sikorska et al. find that remodeling of a GPI anchor after its attachment to proteins inside the ER strongly promotes ER export but occurs independently of protein folding, thereby effectively limiting ER quality control, potentially including ER-associated degradation of all GPI-anchored proteins.

Demonbreun et al. visualized muscle membrane repair in real time after laser-induced microdamage. Annexin proteins were observed to form a repair cap at the site of injury, supporting a shoulder-like structure containing EHD1, EHD2, dysferlin, and MG53.

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