24 research outputs found
Drosophila TIEG Is a Modulator of Different Signalling Pathways Involved in Wing Patterning and Cell Proliferation
Acquisition of a final shape and size during organ development requires a
regulated program of growth and patterning controlled by a complex genetic
network of signalling molecules that must be coordinated to provide positional
information to each cell within the corresponding organ or tissue. The mechanism
by which all these signals are coordinated to yield a final response is not well
understood. Here, I have characterized the Drosophila ortholog
of the human TGF-β Inducible Early Gene 1 (dTIEG). TIEG are zinc-finger
proteins that belong to the Krüppel-like factor (KLF) family and were
initially identified in human osteoblasts and pancreatic tumor cells for the
ability to enhance TGF-β response. Using the developing wing of
Drosophila as “in vivo” model, the dTIEG
function has been studied in the control of cell proliferation and patterning.
These results show that dTIEG can modulate Dpp signalling. Furthermore, dTIEG
also regulates the activity of JAK/STAT pathway suggesting a conserved role of
TIEG proteins as positive regulators of TGF-β signalling and as mediators of
the crosstalk between signalling pathways acting in a same cellular context
Organogenesis and tumorigenesis: Insight from the JAK/STAT pathway in the Drosophila eye
The Janus kinase (JAK) signal transducer and activator of transcription (STAT) pathway is one of the main signaling pathways in eukaryotic cells. This pathway is used during diverse growth and developmental processes in multiple tissues to control cell proliferation, differentiation, survival, and apoptosis. In addition to its role during development, the JAK/STAT pathway has also been implicated in tumorigenesis. Drosophila melanogaster is a powerful genetic tool, and its eyes have been used extensively as a platform to study signaling pathways. Many reports have demonstrated that the JAK/STAT pathway plays pleiotropic roles in Drosophila eye development. Its functions and activation are decided by its interplay with other signal pathways and the epigenetic status. In this review, we focus on the functions and regulation of the JAK/STAT pathway during eye development and provide some insights into the study of this pathway in tumorigenesis. Developmental Dynamics 239:2522–2533, 2010. © 2010 Wiley-Liss, Inc
Validation française du Caregiving Strain Questionnaire sur une population de parents d’enfants avec troubles du spectre de l’autisme
International audienc
Discovery of Transcription Factors and Regulatory Regions Driving In Vivo Tumor Development by ATAC-seq and FAIRE-seq Open Chromatin Profiling
Support Needs of Fathers and Mothers of Children and Adolescents with Autism Spectrum Disorder
Drosophila Myc integrates multiple signaling pathways to regulate intestinal stem cell proliferation during midgut regeneration
High Functioning Autism Spectrum Disorders in Adults: Consequences for Primary Caregivers Compared to Schizophrenia and Depression
A tumor suppressor activity of Drosophila Polycomb genes mediated by JAK-STAT signaling
A prevailing paradigm posits that Polycomb Group (PcG) proteins maintain stem cell identity by repressing differentiation genes, and abundant evidence points to an oncogenic role for PcG proteins in human cancer. Here we show using Drosophila melanogaster that a conventional PcG complex can also have a potent tumor suppressor activity. Mutations in any core PRC1 component cause pronounced hyperproliferation of eye imaginal tissue, accompanied by deregulation of epithelial architecture. The mitogenic JAK-STAT pathway is strongly and specifically activated in mutant tissue; activation is driven by transcriptional upregulation of Unpaired (Upd, also known as Outstretched, Os) family ligands. We show here that upd genes are direct targets of PcG-mediated repression in imaginal discs. Ectopic JAK-STAT activity is sufficient to induce overproliferation, whereas reduction of JAK-STAT activity suppresses the PRC1 mutant tumor phenotype. These findings show that PcG proteins can restrict growth directly by silencing mitogenic signaling pathways, shedding light on an epigenetic mechanism underlying tumor suppression