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Separation of intertwined sister chromatids, mediated by topoisomerase II, is essential for mitosis. In a separate mechanism, phosphorylation of topoisomerase II at Ser 1524 during the G2/M phase of the cell cycle recruits MDC1 to activate the decatenation checkpoint required for genomic stability.
When transplanted into adult mice, purified mouse spermatogonial progenitors that are committed to differentiation can revert to functional germinal stem cells, with the ability to repopulate germ-cell-depleted testes.
Accumulation of amyloid β peptide in cerebral blood vessels has been linked to brain dysfunction. SRF and myocardin transcription factors are induced by cerebral hypoxia and reduce amyloid clearance by regulating SREBP2, a transcriptional repressor that acts on the amyloid aggregate clearance factor LRP1.
The C.elegans anchor cell is a model for cellular invasion through the basement membrane. Now netrin (UNC-6) is found to polarize the actin regulators Ena/VASP and PtdIns (4,5)P2 towards the basement membrane to promote anchor cell invasion.
The midbody ring connects two dividing cells at the end of cytokinesis. Depletion of autophagy components or inhibition of lysosomal function result in accumulation of midbody rings.
As the root develops, auxin transport through non-hair cells sustains root-hair outgrowth. Mathematical modelling and experimental data reveal that auxin is transported through canals across the non-hair cells.
Doubled-stranded DNA breaks activate ATM kinase, precipitating a DNA damage response. The nucleosome-binding protein HMGN1 governs ATM activation by inducing H3K14 acetylation, which regulates chromatin binding of ATM both before and after DSB formation.
Secreted frizzled-related proteins (sFRPs) were reported to antagonise Chordin processing by Sizzled, a tolloid-like metalloproteinase in Xenopus and zebrafish. Surprisingly, mammalian sFRP2 enhances the activity of tolloid-like metalloproteinases on procollagen C to modulate fibrosis associated with cardiac injury.
Incorrectly oriented chromosomes in mitosis can lead to chromosome instability and aneuploidy. The kinesins Kif2b and MCAK stimulate kinetochore-microtubule dynamics to correct mis-orientations.
The guanine nucleotide exchange factor for Ran, RCC1, dynamically binds chromatin. During apoptosis, caspase-mediated activation of Mst1 induces histone H2B phosphorylation, which immobilizes RCC1 on the chromatin, leading to a reduction in nuclear RanGTP.
In cytokinesis, formation of the contractile ring depends on localized activation of RhoA at the cell equator. This study demonstrates that GAP activity of MgcRacGAP is necessary throughout cytokinesis to maintain a focused zone of Rho activity.
The prolyl isomerase Pin1 acts in various cellular processes. It has now been implicated in telomere maintenance by regulating the stability of the telomere binding protein TRF1.
The ubiquitin ligase Siah2 targets HIPK2 kinase for degradation during hypoxia. During normoxia, however, the kinase is stable, as phosphorylation of Siah2 by HIPK2 weakens the interaction.
Septins are cytoskeletal proteins that form a ring at the cytokinetic furrow. Now an analogous 'molecular corset' of septins is found to be required for T lymphocyte migration.
A phosphatidylserine-binding protein, MG53, is shown to participate in membrane repair. MG53 recruits vesicles to the repair site in an oxidation dependent manner and MG53-null mice develop progressive myopathy associated with defective membrane repair.
Neurons and cancer cells metabolize glucose extensively. Intracellular gluthatione produced by this metabolic pathway reduces cytochrome c release from mitochondria to increase cell survival.
The circadian clock is synchronized with the environment. In mammals, besides light input mediated by Per genes, little is known about resetting mechanisms. TGF-β and activin reset the clock by acting on the circadian gene Dec1.
The apoptotic inhibitor IAP1 regulates a feedback loop between the caspase Dronc1 and its apoptosome adaptor Apaf1 to maintain low caspase activity in cells that are not destined to die.
Modelling intracellular force variations at cell protrusions suggests that cell adhesion is regulated at the interface between vinculin and integrin and reveals a putative feedback between increases in tension and F-actin assembly.
Human glioblastoma cells release microvesicles containing a diverse set of proteins, miRNAs and mRNAs, which can be taken up by normal host cells that translate the mRNA. Glioma-derived microvesicles carrying the specific tumour markers EGFRvIII and miRNA-21 promote cell proliferation and may serve as a diagnostic tool.