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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.
Citations are an important component in the assessment of academic performance. Yet, the growing literature, combined with format constraints of journals, encourage citation of reviews in preference to primary research. This diverts academic credit from the discoverer.
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.
Silvio Berlusconi's government seems set on its course to reform Italy's troubled education system through heavy cuts in funding to schools, universities and scientific research, prompting a belated flurry of protests.
A surprising functional association between TRPM3, a mysterious member of the family of transient receptor potential (TRP) cation channels, and the sulphated version of pregnenolone, 'mother' of all steroid hormones, has been identified.
The spindle assembly checkpoint is crucial for maintaining genome integrity in dividing cells by preventing premature chromosome segregation. Degradation of the APC/C activator Cdc20 seems to be an essential and conserved mechanism to maintain this checkpoint in the presence of chromosomes that are not attached to the mitotic spindle.
Studies in Drosophila melanogaster reveal a mechanism for regulating caspases, the key executioners of the apoptotic cell-death program. An initiator caspase and its activating partner promote degradation of each other, thereby limiting the levels of the active protease complex. This negative-feedback inhibition helps to explain how cells avoid unwanted caspase activation and apoptosis.
The tumour suppressor p53 triggers either cell-cycle arrest or apoptosis. Now, arginine methylation joins a panoply of other post-translational modifications that regulate p53. PRMT5 mediates p53 methylation, which disposes the cell to arrest rather than death.
