Induction of Drosophila eye development by decapentaplegic

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 271-278 ◽  
Author(s):  
F. Pignoni ◽  
S.L. Zipursky

The Drosophila decapentaplegic (dpp) gene, encoding a secreted protein of the transforming growth factor-beta (TGF-beta) superfamily, controls proliferation and patterning in diverse tissues, including the eye imaginal disc. Pattern formation in this tissue is initiated at the posterior edge and moves anteriorly as a wave; the front of this wave is called the morphogenetic furrow (MF). Dpp is required for proliferation and initiation of pattern formation at the posterior edge of the eye disc. It has also been suggested that Dpp is the principal mediator of Hedgehog function in driving progression of the MF across the disc. In this paper, ectopic Dpp expression is shown to be sufficient to induce a duplicated eye disc with normal shape, MF progression, neuronal cluster formation and direction of axon outgrowth. Induction of ectopic eye development occurs preferentially along the anterior margin of the eye disc. Ectopic Dpp clones situated away from the margins induce neither proliferation nor patterning. The Dpp signalling pathway is shown to be under tight transcriptional and post-transcriptional control within different spatial domains in the developing eye disc. In addition, Dpp positively controls its own expression and suppresses wingless transcription. In contrast to the wing disc, Dpp does not appear to be the principal mediator of Hedgehog function in the eye.

2011 ◽  
Vol 79 (3) ◽  
pp. 866-874 ◽  
Author(s):  
Markus A. Schirmer ◽  
Jürgen Brockmöller ◽  
Margret Rave-Fränk ◽  
Patricia Virsik ◽  
Barbara Wilken ◽  
...  

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4639-4647 ◽  
Author(s):  
W.M. Deng ◽  
M. Bownes

The Drosophila eggshell, which has a pair of chorionic appendages (dorsal appendages) located asymmetrically along both the anterior/posterior and dorsal/ventral axes, provides a good model to study signal instructed morphogenesis. We show that the Broad-Complex, a gene encoding zinc-finger transcription factors, is essential for the morphogenesis of dorsal appendages and is expressed in a bilaterally symmetrical pattern in the lateral-dorsal-anterior follicle cells during late oogenesis. This is induced and specified along the dorsoventral axis by an epidermal growth factor receptor signalling pathway, which includes a localised transforming growth factor-alpha like molecule, Gurken, in the oocyte and the Drosophila EGF receptor homologue, Torpedo, in the surrounding somatic follicle cells. Furthermore, the precisely localised expression of BR-C along the AP axis requires a separate signalling pathway, initiated by a transforming growth factor-beta homologue, Decapentaplegic, in nearby follicle cells. These two signalling pathways, one from the oocyte and the other from the follicle cells, co-ordinately specify patches of follicle cells to express the Broad-Complex in a unique position in respect to both major axes, which in turn directs the differentiation of the dorsal appendages in the correct position on the eggshell.


2009 ◽  
Vol 18 (20) ◽  
pp. 3969-3977 ◽  
Author(s):  
Mehrnaz Narooie-Nejad ◽  
Seyed Hassan Paylakhi ◽  
Seyedmehdi Shojaee ◽  
Zeinab Fazlali ◽  
Mozhgan Rezaei Kanavi ◽  
...  

ESC CardioMed ◽  
2018 ◽  
pp. 2527-2528
Author(s):  
Charaka Hadinnapola ◽  
Nicholas Morrell

Heritable pulmonary arterial hypertension (PAH) is diagnosed in patients presenting with PAH who have a family history of the disease or carry a mutation in a gene known to be associated with PAH. Heterozygous mutations in the gene encoding the bone morphogenetic protein receptor type 2 (BMPR2) are the most common genetic defects seen in heritable PAH. Mutations in BMPR2 are found in 82% of patients with a family history of PAH and 17% of patients presenting with no family history of the disease. Other causal genes include members of the transforming growth factor beta pathway, including activing receptor-like kinase 1 (ACVRL1) and endoglin (ENG), as well as caveolin 1 (CAV1) and the potassium two-pore domain channel subfamily K member 3 (KCNK3).


Author(s):  
Hong-miao Tao ◽  
Guo-zhong Chen ◽  
Xiao-dong Lu ◽  
Xiao-gang Hu ◽  
Gan-ping Chen ◽  
...  

Background:To clarify the role of inflammation in the pathogenesis of cerebral small vessel disease (SVD), we investigated whether the gene encoding transforming growth factor-beta 1(TGF-beta 1) is a risk factor for cerebral SVD as a whole, and for two different SVD subtypes.Methods:TGF-beta 1 codon10 (T+29C) genotype was determined in 441 Chinese patients (313 male and 128 female) with cerebral SVD and 450 control subjects (326 male and 124 female). Cerebral SVD patients were retrospectively classified into two groups based on neuroimaging findings: lacunar infarction group with 112 patients and ischaemic leukoaraiosis group with 329 patients.Results:Subjects carrying TT homozygote were susceptible to cerebral SVD [adjusted odds ratio (OR) =1.44, 95% confidence interval (CI), 1.05-1.98; P=0.026]. Further analysis of SVD subtypes revealed a moderate association with the ischaemic leukoaraiosis group [OR= 1.60, 95% CI, 1.14-2.25; P=0.007].Conclusions:Codon 10 of TGF-beta 1 might be a risk factor for SVD, specifically in ischaemic leukoaraiosis phenotype.


2020 ◽  
Vol 15 (1) ◽  
pp. 49-55
Author(s):  
Olga Mosunova ◽  
◽  
Elena Dementyeva ◽  

One of the most important representatives of the cytokine family is the transforming growth factor beta 1 (TGF beta 1). The purpose of the review is to study the biological role and clinical significance of TGF beta 1. Using PubMed databases, eLIBRARY, Google Scholar, keywords “cytokines”, “TGF beta 1” found 25,518 sources, 50 selected for analysis. TGF beta 1 is a polyvalent cytokine first isolated from platelets in the 1990s.TGF beta 1 belongs to the family of dimeric polypeptides with a molecular weight of 25 kDa. The gene encoding TGF beta 1 is found in humans on chromosome 19. TGF beta 1 has a pleiotropic effect on the proliferation and differentiation of a wide range of cells, and therefore regulates many physiologic and pathophysiologic processes: immune response, apoptosis, fibrogenesis, and carcinogenesis. TGF beta 1 has an effect on almost all organs and tissues. TGF beta 1 is a key marker that can be used in the diagnosis of a number of diseases. It is necessary to further study the role of TGF beta 1 in the pathophysiologic mechanisms of various diseases, as well as in the development of approaches to targeted therapy.


1994 ◽  
Vol 14 (12) ◽  
pp. 7770-7781 ◽  
Author(s):  
G V Raj ◽  
K Khalili

Immunosuppressive states with accompanying alterations in cytokine profiles have been postulated to play a vital role in the reactivation of viruses from latency. Cytokines regulate gene expression by activating transcription factors via well-characterized signal transduction pathways. In this study, we report the identification of a novel inducible protein, GBP-i, that binds to a double-stranded GGA/C-rich region of the transcriptional control region of the human papovavirus JC virus (JCV), specifically within the origin of viral DNA replication. GBP-i is distinct from previously characterized GC-box-binding proteins with respect to both its sequence specificity and its electrophoretic mobility on native and denaturing gels. GBP-i responds within 90 min to phorbol myristate acetate stimulation; however, unlike typical phorbol myristate acetate-inducible factors, this rapid induction is regulated primarily at the transcriptional level. Further, the induction of GBP-i appears to be widespread and mediated by many inflammatory cytokines, including interleukin-1 beta, tumor necrosis factor alpha, gamma interferon, and transforming growth factor beta. Interestingly, the induced protein acts as a transcriptional repressor in its native context in the JCVL promoter. However, when its binding sequence is transposed to a heterologous promoter, GBP-i appears to function as a transcriptional activator. The data presented here suggest a role for GBP-i in cytokine-mediated induction of viral and cellular genes.


Sign in / Sign up

Export Citation Format

Share Document