29 research outputs found
Developmental Stability: A Major Role for Cyclin G in Drosophila melanogaster
Morphological consistency in metazoans is remarkable given the pervasive occurrence of genetic variation, environmental effects, and developmental noise. Developmental stability, the ability to reduce developmental noise, is a fundamental property of multicellular organisms, yet its genetic bases remains elusive. Imperfect bilateral symmetry, or fluctuating asymmetry, is commonly used to estimate developmental stability. We observed that Drosophila melanogaster overexpressing Cyclin G (CycG) exhibit wing asymmetry clearly detectable by sight. Quantification of wing size and shape using geometric morphometrics reveals that this asymmetry is a genuine—but extreme—fluctuating asymmetry. Overexpression of CycG indeed leads to a 40-fold increase of wing fluctuating asymmetry, which is an unprecedented effect, for any organ and in any animal model, either in wild populations or mutants. This asymmetry effect is not restricted to wings, since femur length is affected as well. Inactivating CycG by RNAi also induces fluctuating asymmetry but to a lesser extent. Investigating the cellular bases of the phenotypic effects of CycG deregulation, we found that misregulation of cell size is predominant in asymmetric flies. In particular, the tight negative correlation between cell size and cell number observed in wild-type flies is impaired when CycG is upregulated. Our results highlight the role of CycG in the control of developmental stability in D. melanogaster. Furthermore, they show that wing developmental stability is normally ensured via compensatory processes between cell growth and cell proliferation. We discuss the possible role of CycG as a hub in a genetic network that controls developmental stability
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
Dimerization of MLL fusion proteins immortalizes hematopoietic cells.
MLL fusion proteins are leukemogenic, but their mechanism is unclear. Induced dimerization of a truncated MLL immortalizes bone marrow and imposes a reversible block on myeloid differentiation associated with upregulation of Hox a7, a9, and Meis1. Both dimerized MLL and exon-duplicated MLL are potent transcriptional activators, suggesting a link between dimerization and partial tandem duplication of DNA binding domains of MLL. Dimerized MLL binds with higher affinity than undimerized MLL to a CpG island within the Hox a9 locus. However, MLL-AF9 is not dimerized in vivo. The data support a model in which either MLL dimerization/exon duplication or fusion to a transcriptional activator results in Hox gene upregulation and ultimately transformation
Dominant modifiers of the polyhomeotic extra-sex-combs phenotype induced by marked P element insertional mutagenesis in Drosophila.
International audienc
Interface effects on the fracture mechanism of a high toughness aluminum composite laminate
The microstructure and the mechanical properties of a multilayer composite
laminate based on aluminum 7075 and 2024 alloys produced by hot roll-bonding were
examined. The composite laminate has been tested at room temperature under impact
Charpy tests, three-point bend tests and shear tests on the interfaces. The toughness of
the post-rolling tempered and T6 treated composite laminate, measured by impact
absorbed energy in the crack arrester orientation, was more than twenty times higher
than that of the monolithic Al 7075 alloy and seven times higher than that of Al 2024
alloy. The outstanding toughness increase of the composite laminate in the post-rolling
tempered and T6 treated condition is mainly due to the mechanism of “interface predelamination”.
By this fracture mechanism the interfaces are debonded before the main
crack reaches them, warranting delamination in all interfaces. Therefore, delamination
and crack renucleation in every layer are responsible for the improvement in toughness.Financial support from CICYT (Project MAT2003-01172) is gratefully acknowledged.
C.M. Cepeda-JimĂ©nez and J.M. GarcĂa-Infanta thank the Spanish Ministry of Education and
Science for a Juan de la Cierva contract and a FPI fellowship respectively. We also thank L. del
Real-AlarcĂłn for the welding work, F.F. González-RodrĂguez for assistance during hot rolling
and J. Chao-Hermida for assistance with the Charpy impact test.Peer reviewe