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The impact of the continuing economic woes on science funding remains uncertain. Surprisingly, the crisis may actually reinvigorate research. Investment in science and education is a prerequisite not only for emergence from the economic downward spiral, but also for addressing pressing global needs.
Prions are abnormal isoforms of host proteins that are the infectious agents in certain mammalian neurodegenerative diseases. How prions travel from their peripheral entry sites to the brain where they cause disease is poorly understood. A new study finds that tunnelling nanotubes are important for the intercellular transfer of prions during neuroinvasion.
Frizzled receptors regulate cell fate decisions and planar cell polarity by means of distinct intracellular effectors. The choice between these two signalling outputs may involve a pH-dependent interaction between Dishevelled and negatively charged lipids at the plasma membrane.
Tumorigenesis is regulated by several mechanisms including signalling, transcription and DNA replication. Now a cytoplasmic protein quality-control pathway is implicated in the suppression of breast cancer cell growth, suggesting a new role for quality-control mechanisms in suppressing cells with malignant potential.
Epigenetic mechanisms participate in the regulation of gene transcription in eukaryotes. Two studies in yeast have revealed an additional mechanism for controlling global gene transcription that is based on an inherited self-perpetuating change in the conformation of two different components of key transcriptional regulatory complexes.
The growth of daughter cells in budding yeast is a classic model for investigating mechanisms involved in asymmetric cell division. An unexpected collaboration between the DEAD-box protein Dbp5 and the nuclear transport receptor Kap104 controls localized protein synthesis at the bud tip during mitosis.
Lamin B is a component of a membranous matrix thought to be essential for spindle assembly. The dynein motor and its interacting protein Nudel are required for the recruitment of lamin B to the spindle matrix.
By preventing G-actin accumulation, Rho-GTPase promotes the transcriptional activity of myocardin-related transcription factors (MRTFs), known co-factors of serum response factor (SRF). Rho-dependent MRTF expression is required for injected metastatic cell lines to colonize the lung.
LIN-5 acts at the cortex with Ga to control spindle positioning but is also localized at spindle poles. The LIN-5 interacting protein ASPM-1 and calmodulin are required for its recruitment to spindle poles and the LIN-5/ASPM-1/calmodulin complex regulates meiotic spindle positioning.
Double-strand breaks in DNA activate the kinases ATM and ATR, which block entry into mitosis. ATM and ATR also delay mitotic progression by controlling spindle assembly in Xenopus egg extracts through the phosphorylation of the centrosomal protein CEP63, leading to its delocalization from the centrosome.
A genome-wide RNAi screen reveals the importance of local pH regulation during planar epithelial polarization. The plasma membrane association of the planar cell polarity components Dishevelled/Frizzled depends on the activity of the Na+/H+ membrane exchanger Nhe2.
The ubiquitin ligase Chfr polyubiquitylates the histone deacetylase Hdac1, resulting in its proteolysis and the concomitant upregulation of metastasis suppressors, which may provide a molecular explanation for the known effects of Chfr on tumour progression.
Live-cell imaging shows that haematopoietic progenitor cells contact osteoblasts through a specialized membrane domain that is consequently internalized by osteoblasts. This results in downregulation of Smad signalling and the production of chemokines by osteoblasts that stimulate haematopoietic progenitor cell homing to bone marrow.
The ubiquitin ligase CHIP suppresses tumour growth and metastasis in breast cancer, and its expression inversely correlates with malignancy. The role of CHIP in cancer depends on degradation of the transcriptional co-activator SRC-3, which regulates expression of Smad and Twist.
Cancer cells characteristically undergo a shift from oxidative to glycolytic metabolism. Loss of the transcription factor Oct1 opposes tumorigenicity by inducing a coordinate metabolic shift from glucose metabolism to increased mitochondrial activity and amino acid oxidation.
Tunnelling nanotubes provide a means of intercellular communication. They are now shown to facilitate spreading of prions between neuronal cells, as well as their propagation from dentritic cells to primary neurons.
The molecular determinants of gating and regulation of the calcium channel Orai1 by the ER Ca2+ sensor STIM1 during store-operated calcium entry are now defined.
The transcriptional activator SWI was recently shown to propagate as a prion in yeast. Cyc8, a co-repressor that regulates a similar set of genes as SWI, also propagates as a prion, suggesting a link between chromatin remodelling and cytoplasmic inheritance of prion traits.
The intracellular localization of the karyopherin KAP104 determines where dissociation of the mRNA binding proteins Nab2 and Nab4 from translation competent mRNAs takes place, thus controlling local protein synthesis.
The replication of heterochromatic chromosome regions is temporally regulated. The yeast heterochromatin protein Swi6 (mammalian HP1) activates replication origins by recruiting the kinase Dfp1, which facilitates loading of replication factor Sld3 on early replicating heterochromatin.