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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.
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.
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.
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.
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.
The anti-apoptotic regulators XIAP and c-IAPs promote turnover of the cRAF kinase to control cell migration. XIAP binding facilitates ubiquitylation of cRAF through the ubiquitin ligase CHIP.
P-ATPases in plants are typically thought to act at the plasma membrane. In contrast, PH5, a P-type H+ ATPase functions within the vacuolar membrane to control acidification during flower coloration.
The general transcription factor TATA-binding protein (TBP) is retained at gene promoters during mitosis, where it recruits PP2A to inactivate condensin. Chromatin decondensation at promoters may be associated with gene bookmarking, a mechanism to re-establish gene activity patterns in daughter cells.
A ubiquitin binding domain in the IAP proteins binds Lys 63-linked poly-ubiquitin chains and is essential for the oncogenic potential of cIAP. This domain is also required for activating NF-κB, possibly by binding poly-ubiquitinated NEMO.
In a kinase-independent manner, PAK1 serves as a scaffold that regulates Akt recruitment to the membrane and its stimulation by PDK1, thus regulating efficiency, localization and specificity of the PDK1–Akt pathway.
Mono-ubiquitylation of histone H2B is required for methylation of histone H3K4. Ubiquitylation of H2B in turn promotes ubiquitylation of Swd2, a component of the SET1/COMPASS methyltransferase. Inhibiting Swd2 ubiquitylation impairs recruitment of the COMPASS subunit, which is essential for methylation, and results in reduced H3K4 methylation.
Abnormal relocalization of A-type lamins to the nuclear envelope in LAP2α-deficient mice impairs pRb-mediated regulation of progenitor cell proliferation and differentiation in highly regenerative tissues.