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Silencing of rRNA is an ATM-dependent pan-nuclear response to irradiation in which the DNA damage protein Nbs1 accumulates in nucleoli, through binding to the nucleolar protein Treacle.
Mitosis depends upon the action of the mitotic spindle, a subcellular machine that uses microtubules (MTs) and motors to assemble itself and to coordinate chromosome segregation. Recent work illuminates how the motor-driven poleward sliding of MTs — nucleated at centrosomes, chromosomes and on pre-existing MTs — contributes to spindle assembly and length control.
Chromosome instability is a major hallmark of cancer, but its molecular causes are still poorly understood. A study now describes how genetic alterations frequently found in colorectal cancer increase microtubule assembly rates during mitosis and promote chromosome instability.
Anti-tubulin drugs are life-saving chemotherapeutics that kill cancer cells by stabilizing or disrupting microtubules. Despite their clinical utility, the molecular mechanisms by which anti-tubulins cause apoptotic cell death remain poorly understood. It is now shown that microtubule disruption can inhibit anti-apoptotic Bcl-2 family proteins through an evolutionarily conserved signalling axis involving DEPDC1 (LET-99 in Caenorhabditis elegans) and JNK.
Lgr5, a marker of stem cells in many organs, is found expressed in cells scattered through the ovarian epithelium that expand to repair and regenerate the damaged ovarian surface after each ovulation. Lgr5-positive stem cells in the ovary and the fimbria of the oviduct may be critical cells of origin for ovarian cancer.
The ovary surface epithelium undergoes ovulation-induced tear and remodelling. Barker and colleagues have identified Lgr5-expressing stem cells in the mouse ovary and show that they contribute to ovary organogenesis as well as participate in epithelial repair throughout life.
During embryogenesis, the single layer of mouse epidermal progenitors becomes a stratified and differentiated epithelium. Fuchs and colleagues show that the polarity proteins Par3–mInsc and Gαi3 act cooperatively to polarize LGN and promote perpendicular divisions to induce stratification.
How microtubule minus ends are organized during spindle assembly has remained unclear. Lecland and Lüders demonstrate that γ-tubulin ring complexes associate with non-centrosomal minus ends, and that minus ends are transported towards spindle poles in a manner dependent on the microtubule motors dynein, HSET and Eg5.
Chromosomal instability (CIN) is a common feature of colorectal cancer cells and several mechanisms have been suggested for CIN generation. Bastians and colleagues find that increased microtubule plus-end stability can be triggered by AURKA overexpression and is associated with abnormal spindles and lagging chromosomes in colorectal cancer cells.
DNA damage induces silencing of ribosomal RNA (rRNA) transcription. Stucki and colleagues reveal that rRNA silencing is an ATM-dependent pan-nuclear response to irradiation, in which the nucleolar protein Treacle targets DNA-damage protein NBS1 to nucleoli.
The motor protein dynein binds growing microtubule ends, but how it is recruited to plus ends has not been clear. Using in vitro reconstitution and TIRF microscopy, Surrey and colleagues identify a recruitment pathway in which the plus-end binding protein EB1 binds CLIP-170, which in turn recruits the p150 dynein subunit.
Hengartner and colleagues use an RNAi-based screening approach in C. elegans to identify effectors of the chemotherapy drug vincristine. They report that the drug induces apoptosis by targeting a conserved LET-99–GPA-11–JNK1 pathway.
