Skip to content
Login Register

#nuclear envelope breakdown

2 public questions tagged with this topic.

Cell Cycle Regulation

How do mitotic CDKs promote nuclear envelope breakdown?

Interphase nucleus bounded by double membrane supported by lamina composed of type V intermediate filaments lamin A/C, B1, B2 forming meshwork under inner nuclear membrane and linking to chromatin via emerin, LAP2 beta and LBR. Breakdown necessary for spindle access in metazoa relies on mitotic CDK1-Cyclin B catalyzed phosphorylation. CDK1 phosphorylates lamins at conserved sites flanking central alpha-helical rod: Ser22 and Ser392 on Lamin A/C cause electrostatic repulsion and disassembly of head-to-tail polymers into soluble dimers and tetramers. Concurrently CDK1 and Plk1 phosphorylate nucl

Ref: Guttinger et al., Mechanisms of Nuclear Envelope Breakdown and Reformation, Nat Rev Mol Cell Biol 2009; Alberts, Chapter 17.

View Details
Cell Cycle Regulation

The mitotic CDK1-Cyclin B complex (MPF) is responsible for:

MPF converts interphase architecture into mitotic state through phosphorylation of hundreds of substrates. Nuclear entry of CDK1-Cyclin B, facilitated by phosphorylation of Cyclin B cytoplasmic retention sequence, allows access to chromatin proteins. Condensin I and II pentameric complexes containing SMC2, SMC4 become phosphorylated at non-SMC subunits CAP-D2, D3, CAP-G, H2, activating ATP-dependent loop extrusion that folds 10nm fiber into 700 nm wide rod chromosomes. Lamins phosphorylated at Ser22 Ser392 disassemble intermediate filament meshwork leading to nuclear envelope breakdown and mer

Ref: Hirano, Condensins and Mitotic Chromosome Architecture, Nat Rev Mol Cell Biol 2012; Alberts et al., Chapter 17, MPF Targets.

View Details