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Multiple processes in the cell require curved membranes. Stachowiak, Brodsky and Miller discuss how lipids and vesicle cargo proteins represent energy barriers to membrane bending, and how different mechanisms may operate to overcome these barriers as drivers of membrane curvature.
Faithful genome segregation depends on the functions of the eukaryotic centromere, which is characterized by the histone variant CENP-A. Gene replacement in human cells and fission yeast has now been used to show how CENP-A biochemically encodes centromere identity, as well as reveal an unexpected role for CENP-B in centromere function.
During mitosis, kinetochores attach to microtubule plus ends, thus allowing dynamic microtubules to properly segregate chromosomes. How this type of 'end-on' attachment between microtubule plus ends and kinetochores is formed and maintained is unclear. CENP-E, a kinesin-7 family member, is now shown to have a role in associating kinetochores with dynamic microtubule plus ends.
Carroll and colleagues show that the atypical cadherin Fat4 derived from stromal fibroblasts cooperates with Wnt9b produced by the ureteric bud to modulate self-renewal and differentiation of kidney progenitors.
Upstream inputs providing directional bias in cellular polarity within the plane of an epithelium (PCP) remain unclear. Mlodzik and colleagues found that the Wnt ligand Wingless and Drosophila Wnt homologue dWnt4 establish the PCP axis perpendicular to their expression domain through modulating interactions between the recognized core PCP components Frizzled and Van Gogh.
The centromere-specific histone H3 variant CENP-A is sufficient for centromere specification in many species. Cleveland and colleagues have used an elegant gene targeting strategy to define a two-step mechanism for how CENP-A acts in centromere targeting and kinetochore assembly and function.
Autophagy, which is believed to be an Atg7- and Atg3-dependent process, is known to be involved in animal development. Baehrecke and colleagues show that autophagy drives the controlled degradation of the developing Drosophila midgut. Interestingly, this process is Atg7- and Atg3-independent, and instead requires the E1-activating enzyme Uba1 for programmed reduction of cell size in the midgut.
Grishchuk and colleagues report that CENP-E, which is known to transport chromosomes towards the plus end of spindle microtubules, is also able to track microtubule tips bi-directionally.
Oct4 is a core component of the regulatory network of pluripotency. Schöler and colleagues found that establishment of totipotency was not affected by genetic elimination of maternal Oct4a, with live offspring being born and oocytes able to reprogram somatic cell nuclei. However, ablation of both maternal and zygotic Oct4a led to the formation of an inner cell mass that was not pluripotent.
The mammalian heart is formed from two distinct groups of mesodermal cells, the first and second heart fields (FHF and SHF). Little is known about the progenitors giving rise to the FHF, but Chien and colleagues have now identified HCN4 (hyperpolarization-activated cyclic nucleotide-gated channel 4) as an FHF marker. They show by lineage tracing that cells expressing HCN4 primarily contribute to cardiomyogenic lineages, and use this marker to isolate FHF progenitors from differentiation cultures of human embryonic stem cells.
It has been shown that planar cell polarity (PCP) signalling and cilium positioning are linked. Montcouquiol and colleagues now show that G-protein signalling, through the GTP-binding G-protein subunit Gαi3 and the apicobasal polarity protein mPins, modulates cilium positioning cell autonomously. They also show that PCP signalling controls cilium positioning at the tissue level.
Hyman and colleagues modulate the activity of the XMAP215 microtubule polymerase and show that spindle length is proportional to the maximum microtubule growth velocity set by XMAP215.
Niethammer and colleagues report that leukocytes are recruited to damaged tissue sites in zebrafish through an osmotic signalling network that responds to changes in osmolarity between the interstitial fluid and the external environment.
