The Enhancer of Trithorax and Polycomb Corto Interacts with Cyclin G in Drosophila

BACKGROUND: Polycomb (PcG) and trithorax (trxG) genes encode proteins involved in the maintenance of gene expression patterns, notably Hox genes, throughout development. PcG proteins are required for long-term gene repression whereas TrxG proteins are positive regulators that counteract PcG action. PcG and TrxG proteins form large complexes that bind chromatin at overlapping sites called Polycomb and Trithorax Response Elements (PRE/TRE). A third class of proteins, so-called "Enhancers of Trithorax and Polycomb" (ETP), interacts with either complexes, behaving sometimes as repressors and sometimes as activators. The role of ETP proteins is largely unknown. METHODOLOGY/PRINCIPAL FINDINGS: In a two-hybrid screen, we identified Cyclin G (CycG) as a partner of the Drosophila ETP Corto. Inactivation of CycG by RNA interference highlights its essential role during development. We show here that Corto and CycG directly interact and bind to each other in embryos and S2 cells. Moreover, CycG is targeted to polytene chromosomes where it co-localizes at multiple sites with Corto and with the PcG factor Polyhomeotic (PH). We observed that corto is involved in maintaining Abd-B repression outside its normal expression domain in embryos. This could be achieved by association between Corto and CycG since both proteins bind the regulatory element iab-7 PRE and the promoter of the Abd-B gene. CONCLUSIONS/SIGNIFICANCE: Our results suggest that CycG could regulate the activity of Corto at chromatin and thus be involved in changing Corto from an Enhancer of TrxG into an Enhancer of PcG

Aggregate Selection in Evolutionary Robotics

Can the processes of natural evolution be mimicked to create robots or autonomous agents? This question embodies the most fundamental goals of evolutionary robotics (ER). ER is a field of research that explores the use of artificial evolution and evolutionary computing for learning of control in autonomous robots, and in autonomous agents in general. In a typical ER experiment, robots, or more precisely their control systems, are evolved to perform a given task in which they must interact dynamically with their environment. Controllers compete in the environment and are selected and propagated based on their ability (or fitness) to perform the desired task. A key component of this process is the manner in which the fitness of the evolving controllers is measured. In ER, fitness is measured by a fitness function or objective function. This function applies some given criteria to determine which robots or agents are better at performing the task for which they are being evolved. Fitness functions can introduce varying levels of a priori knowledge into evolving populations. Som

Siamois functions in the early blastula to induce Spemann's organiser

International audienceIn Xenopus, the Spemann organiser is defined as a dorsal territory in the early gastrula that initiates development of the embryonic axis. It has been shown that the early zygotic transcription factor Siamois is essential for Spemann's organiser formation. By the onset of gastrulation, the organiser is patterned into a vegetal head organiser, which induces anterior structures upon transplantation, and a more animal trunk organiser, which induces a posterior neuraxis. However, it is unclear when these distinct organiser domains are initially specified. To shed light on this question, we analysed the temporal activity of Siamois, as this factor induces both head and trunk development, when ectopically expressed via mRNA injection. In this study, we expressed Siamois ectopically at different time points and analysed the extent of axial development. Using a hormone- inducible version of Siamois, we found evidence for a tight window of competence during which ventral cells can respond to Siamois by commencing both the head and the trunk genetic programmes. The competence to form Spemann's organiser was lost 2 h before gastrulation, although partial axis formation could still occur following delayed activation of Siamois. We demonstrate that this late response to Siamois involves a new role for this gene, which can indirectly repress ventral gene expression, in the absence of known organiser genes. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved

Distinct Xenopus Nodal ligands sequentially induce mesendoderm and control gastrulation movements in parallel to the Wnt/PCP pathway

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MicroRNAs as key regulators of GTPase-mediated apical actin reorganization in multiciliated epithelia

International audienceMulticiliated cells (MCCs), which are present in specialized vertebrate tissues such as mucociliary epithelia, project hundreds of motile cilia from their apical membrane. Coordinated ciliary beating in MCCs contributes to fluid propulsion in several biological processes. In a previous work, we demonstrated that microRNAs of the miR-34/449 family act as new conserved regulators of MCC differentiation by specifically repressing cell cycle genes and the Notch pathway. Recently, we have shown that miR-34/449 also modulate small GTPase pathways to promote, in a later stage of differentiation, the assembly of the apical actin network, a prerequisite for proper anchoring of centrioles-derived neo-synthesized basal bodies. We characterized several miR-34/449 targets related to small GTPase pathways including R-Ras, which represents a key and conserved regulator during MCC differentiation. Direct RRAS repression by miR-34/449 is necessary for apical actin meshwork assembly, notably by allowing the apical relocalization of the actin binding protein Filamin-A near basal bodies. Our studies establish miR-34/449 as central players that orchestrate several steps of MCC differentiation program by regulating distinct signaling pathways

MicroRNAs as key regulators of GTPase-mediated apical actin reorganization in multiciliated epithelia

International audienceMulticiliated cells (MCCs), which are present in specialized vertebrate tissues such as mucociliary epithelia, project hundreds of motile cilia from their apical membrane. Coordinated ciliary beating in MCCs contributes to fluid propulsion in several biological processes. In a previous work, we demonstrated that microRNAs of the miR-34/449 family act as new conserved regulators of MCC differentiation by specifically repressing cell cycle genes and the Notch pathway. Recently, we have shown that miR-34/449 also modulate small GTPase pathways to promote, in a later stage of differentiation, the assembly of the apical actin network, a prerequisite for proper anchoring of centrioles-derived neo-synthesized basal bodies. We characterized several miR-34/449 targets related to small GTPase pathways including R-Ras, which represents a key and conserved regulator during MCC differentiation. Direct RRAS repression by miR-34/449 is necessary for apical actin meshwork assembly, notably by allowing the apical relocalization of the actin binding protein Filamin-A near basal bodies. Our studies establish miR-34/449 as central players that orchestrate several steps of MCC differentiation program by regulating distinct signaling pathways

MicroRNA-based silencing of Delta/Notch signaling promotes multiple cilia formation

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Mutations in ccf, a novel Drosophila gene encoding a chromosomal factor, affect progression through mitosis and interact with Pc-G mutations.

We report herein the isolation of ccf, a new gene located in region 82E and essential for Drosophila development. This gene, expressed throughout development, encodes a novel product of 68 kDa which is found in the nucleus during interphase and labels, in a novel pattern, centrosomes and chromosome arms during mitosis. Mutations in ccf give rise to late larvae with small imaginal discs and to adults showing appendages of reduced size, consistent with CCF involvement in cell proliferation. Neuroblast squash analyses show that CCF is required for proper condensation of mitotic chromosomes and, therefore, for progression through mitosis. Furthermore, we observe that adult ccf mutants as well as animals overexpressing CCF during larval stages exhibit homeotic transformations. We also find that mutations in the Pc-G genes Polycomb, polyhomeotic and Enhancer of zeste are enhanced by ccf mutations. Finally, we show that the CCF protein binds to specific sites on polytene chromosomes, many of which are shared with the Posterior sex combs Pc-G protein. Together, these results suggest a role for the CCF protein in the maintenance of chromosome structure during mitosis and interphase