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A confocal section through a mouse embryonic hair follicle that has lost asymmetry due to a mutation in the Vangl2 gene. E-Cadherin (red) marks cell borders, Celsr1 (green) is abnormally diffuse.
This year's Nobel Prizes mark the most significant technological advance in cell biology, GFP et al., as well as two discoveries in virology with major health implications.
Trans-tail regulation is the linked post-translational modification of tails on different histones. Two important studies implicate Swd2 as the link between H2B ubiquitylation and H3 methylation. Swd2 is a component of both the SET1 methyltransferase complex and the cleavage and polyadenylation factor CPF, implicating trans-tail regulation in differentiating events at the beginning and end of genes.
Mammalian hairs have characteristic patterns of orientation, with a predominantly rostral to caudal direction, occasional swirls and a high level of local correlation between hairs. A detailed new study demonstrates that the polarity of hairs derives from an underlying planar polarity of the basal epidermal cells from which hair follicles arise.
The balance between proliferation and differentiation is essential not only for the generation and maintenance of tissues, but also to prevent uncontrolled cell division and tumorigenesis. The mitotic kinase Aurora A coordinates cell-cycle events and asymmetric division by regulating localization of the cell fate determinant Numb through remodelling of the conserved PAR polarity complex.
Mammalian hair follicles are aligned along the anterior–posterior axis. The planar cell polarity genes Vangl2 and Celsr1 are essential for hair follicle polarization and orientation.
The large, multi-functional protein DENN/MADD is an important linker between Rab3 and the kinesin-3 motor proteins KIF1Bβ and KIF1A in the transport of synaptic vesicle precursors.
A genome-wide screen reveals that the transcription factor Elf5 is epigenetically silenced in the embryonic cell lineage and that its expression is restricted to the trophoblast, where it creates a positive-feedback loop with Cdx2 and Eomes.
The chromatin mark H3K27me3 is transmitted during cell division by recruitment and binding of the PRC2 complex, which maintains the mark and leads to methylation of H3K27 on newly incorporated histones.
In mammalian oocytes, cell polarity is established when meiosis I chromosomes move from the egg centre to the cortex. This translocation is dependent on actin filaments trailing behind the chromosomes, and on the actin-nucleating activity of the formin Fmn2.
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.
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.
ING proteins bind to lamin A. ING1 expression and localization is perturbed in lamin A-null cells. Data from Hutchinson-Gilford progeria syndrome (HGPS) cells, which carry mutations in lamin A, suggest that loss of lamin A–ING interaction may contribute to the HGPS phenotype.
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.
The production of chemoattractants in the pre-metastatic lung can be induced by distant primary tumours. The chemoattractants S100A8 and S100A9 induce serum amyloid A3 and TLR4 activation and cause an inflammation-like state that facilitates metastasis.
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.
