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Exosomes are endosome-derived membrane vesicles that are key for intercellular communication in the immune system and elsewhere. Rab27A and Rab27B GTPases and two of their cognate effector proteins seem to be needed to drive the physiologically important exosome-release process in certain cell types.
During development, proliferating cells are organized into compartments with boundaries across which cells fail to intermix. Compartment boundaries are often attributed to differential cell–cell adhesion between separate compartments. However, tension generated by actomyosin cables at boundaries can also function as a barrier that prevents cell mixing.
Cdk2 has been shown to have an unanticipated role in suppressing Myc-induced senescence. This has implications for how c-Myc overcomes failsafe mechanisms to induce tumorigenesis and suggests that the inhibition of Cdk2 may have therapeutic efficacy in the treatment of cancer.
It is unclear whether viral particles can induce membrane curvature. Binding of Simian virus 40 (SV40) to the GM1 ganglioside on host plasma membranes leads to membrane curvature and the formation of invaginations in cells and in giant unilamellar vesicles, an effect required for viral infection.
Exosome biogenesis is poorly understood. The small GTPases Rab27a and Rab27b and their effectors, Slp4 and Slac2b, control exosome secretion at different steps by regulating the peripheral localization, retention and docking of exosomal precursors, the multivesicular endosomes.
The Wnt/b-catenin pathway controls proliferation and self-renewal of mouse adult neural stem cells, and the nuclear receptor TLX is shown to activate this pathway by inducing expression of Wnt7. Thus, neural stem cells promote their own self-renewal by secreting signalling molecules that act in an autocrine and paracrine mode.
Mouse mutants for Sec24b, a component of COPII-coated ER-to-Golgi vesicles, have defects in convergent extension, neural tube closure and other phenotypes related to planar cell polarity (PCP). The PCP component Vangl2 is sorted by Sec24b, and Vangl2 mutants defective in convergent extension do not exit the ER.
During germ-cell migration in the zebrafish embryo, Rac1 and RhoA are activated at the cell front where they control formation of actin structures and retrograde flow, respectively. This is imperative for the control of E-cadherin-mediated traction forces that drive single cell migration.
Cyclin-dependent kinase 2 (cdk2) is surprisingly found to suppress senescence induced by the Myc oncogene in various cell types. Inactivation or deletion of cdk2 sensitizes mouse embryonic fibroblasts to Myc-induced senescence via a mechanism requiring pRb and p53.
The molecular and cellular mechanisms that keep cells apart at compartment boundaries remain unclear. In early Drosophila embryos, cells transiently invade neighbouring compartments, but an actomyosin-based barrier formed of cable-like structures pushes them back into their compartment of origin, in mitotically active epidermis.
Shigella infection can lead to stimulation of the NF-κB pathway. IpaH9.8, a Shigella effector with ubiquitin ligase activity polyubiquitylates NEMO, a key regulator of NF-κB activation, leading to its degradation and subsequent impairment of NF-κB activation.
DNA ligase I links newly synthesized DNA fragments. DNA ligase I deficiency causes ubiquitylation of PCNA in yeast and human by the E2 variant Mms26, Ubc47 and the E3 Rad5, which is required for activation of the DNA damage response and cell viability.
HERC2 regulates the retention of repair proteins 53BP1, RAP80 and BRCA1 on damaged chromosomes in response to ionizing radiation by forming a complex with the ubiquitin ligases RNF8 and RNF168. Hecr2 deficiency leads to radiosensitivity.
In response to CO2, leaves close their stomatal pores but the CO2-binding proteins and the cell type responsible for this effect have not been identified. Expression of β-carbonic anhydrase in guard cells modulates the CO2-mediated regulation of stomatal movements.
Small RNAs are known to induce heterochromatin formation in various organisms. RNA-dependent mechanisms are shown to be required for the formation of a constitutive heterochromatin structure in the chick.
