mtv shapes the activity gradient of the Dpp morphogen through regulation of thickveins

Development ◽  
2001 ◽  
Vol 128 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Y. Funakoshi ◽  
M. Minami ◽  
T. Tabata
Keyword(s):  
Expression Pattern ◽  
Regulatory Mechanism ◽  
Major Type ◽  
Type I ◽  
Posterior Compartment ◽  
Novel Gene ◽  
Compartment Boundary

Drosophila wings are patterned by a morphogen, Decapentaplegic (Dpp), a member of the TGFbeta superfamily, which is expressed along the anterior and posterior compartment boundary. The distribution and activity of Dpp signaling is controlled in part by the level of expression of its major type I receptor, thickveins (tkv). The level of tkv is dynamically regulated by En and Hh. We have identified a novel gene, master of thickveins (mtv), which downregulates expression of tkv in response to Hh and En. mtv expression is controlled by En and Hh, and is complementary to tkv expression. In this report, we demonstrate that mtv integrates the activities of En and Hh that shape tkv expression pattern. Thus, mtv plays a key part of regulatory mechanism that makes the activity gradient of the Dpp morphogen.

Signaling through both type I DPP receptors is required for anterior-posterior patterning of the entire Drosophila wing

Development ◽  
1997 ◽  
Vol 124 (1) ◽  
pp. 79-89 ◽  
Author(s):  
M.A. Singer ◽  
A. Penton ◽  
V. Twombly ◽  
F.M. Hoffmann ◽  
W.M. Gelbart
Keyword(s):  
Cell Fate ◽  
Type I ◽  
Posterior Compartment ◽  
Anterior Compartment ◽  
Hypomorphic Allele ◽  
Compartment Boundary ◽  
Adult Wing ◽  
Mutant Cells ◽  
Narrow Stripe ◽  
Anterior Posterior

The imaginal disk expression of the TGF-beta superfamily member DPP in a narrow stripe of cells along the anterior-posterior compartment boundary is essential for proper growth and patterning of the Drosophila appendages. We examine DPP receptor function to understand how this localized DPP expression produces its global effects upon appendage development. Clones of saxophone (sax) or thick veins (tkv) mutant cells, defective in one of the two type I receptors for DPP, show shifts in cell fate along the anterior-posterior axis. In the adult wing, clones that are homozygous for a null allele of sax or a hypomorphic allele of tkv show shifts to more anterior fates when the clone is in the anterior compartment and to more posterior fates when the clone is in the posterior compartment. The effect of these clones upon the expression pattern of the downstream gene spalt-major also correlates with these specific shifts in cell fate. The similar effects of sax null and tkv hypomorphic clones indicate that the primary difference in the function of these two receptors during wing patterning is that TKV transmits more of the DPP signal than does SAX. Our results are consistent with a model in which a gradient of DPP reaches all cells in the developing wing blade to direct anterior-posterior pattern.

Role of knot (kn) in Wing Patterning in Drosophila

Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1203-1212 ◽  
Author(s):  
Katerina Nestoras ◽  
Helena Lee ◽  
Jym Mohler
Keyword(s):  
Hedgehog Signaling ◽  
Imaginal Disc ◽  
Hedgehog Signaling Pathway ◽  
Posterior Compartment ◽  
Drosophila Wing ◽  
Compartment Boundary ◽  
Hh Signaling ◽  
Embryonic Segmentation ◽  
Anterior Posterior

We have undertaken a genetic analysis of new strong alleles of knot (kn). The original kn1 mutation causes an alteration of wing patterning similar to that associated with mutations of fused (fu), an apparent fusion of veins 3 and 4 in the wing. However, unlike fu, strong kn mutations do not affect embryonic segmentation and indicate that kn is not a component of a general Hh (Hedgehog)-signaling pathway. Instead we find that kn has a specific role in those cells of the wing imaginal disc that are subject to ptc-mediated Hh-signaling. Our results suggest a model for patterning the medial portion of the Drosophila wing, whereby the separation of veins 3 and 4 is maintained by kn activation in the intervening region in response to Hh-signaling across the adjacent anterior-posterior compartment boundary.

scholarly journals Protein modification with ISG15 blocks coxsackievirus pathology by antiviral and metabolic reprogramming

2020 ◽  
Vol 6 (11) ◽  
pp. eaay1109 ◽  
Author(s):  
Meike Kespohl ◽  
Clara Bredow ◽  
Karin Klingel ◽  
Martin Voß ◽  
Anna Paeschke ◽  
...  
Keyword(s):  
Protein Modification ◽  
Shotgun Proteomics ◽  
Oxidative Capacity ◽  
Metabolic Reprogramming ◽  
Major Type ◽  
Infection Model ◽  
Type I ◽  
Synergistic Activity ◽  
Cardiac Damage ◽  
Species Specific

Protein modification with ISG15 (ISGylation) represents a major type I IFN–induced antimicrobial system. Common mechanisms of action and species-specific aspects of ISGylation, however, are still ill defined and controversial. We used a multiphasic coxsackievirus B3 (CV) infection model with a first wave resulting in hepatic injury of the liver, followed by a second wave culminating in cardiac damage. This study shows that ISGylation sets nonhematopoietic cells into a resistant state, being indispensable for CV control, which is accomplished by synergistic activity of ISG15 on antiviral IFIT1/3 proteins. Concurrent with altered energy demands, ISG15 also adapts liver metabolism during infection. Shotgun proteomics, in combination with metabolic network modeling, revealed that ISG15 increases the oxidative capacity and promotes gluconeogenesis in liver cells. Cells lacking the activity of the ISG15-specific protease USP18 exhibit increased resistance to clinically relevant CV strains, therefore suggesting that stabilizing ISGylation by inhibiting USP18 could be exploited for CV-associated human pathologies.

scholarly journals PADI3 plays an antitumor role via the Hsp90/CKS1 pathway in colon cancer

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhengbin Chai ◽  
Li Wang ◽  
Yabing Zheng ◽  
Na Liang ◽  
Xiwei Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Expression Pattern ◽  
Colony Formation ◽  
Regulatory Mechanism ◽  
Cancer Cell Proliferation ◽  
Colon Cancer Cells ◽  
Cancer Tissues

Abstract Background CKS1 is highly expressed in colon cancer tissues, and is essential for cancer cell proliferation. The downstream molecular mechanism of CKS1 has been fully studied, but the upstream regulatory mechanism of it is still unclear. Earlier research found that PADI3 plays its anti-tumor roles via suppress cell proliferation, in this study, we found that the expression pattern of PADI3 and CKS1 are negatively correlated in colon cancer tissues, and overexpression of PADI3 can partly reverse CKS1 induced cancer cell proliferation. However, the regulatory mechanism of PADI3 and CKS1 in the tumorigenesis of colon cancer is still unclear and need to do further research. Methods Western blot and real-time PCR were used to detect the expression levels of genes. CCK-8 and colony formation assays were used to examine cell proliferation and colony formation ability. Overexpression and rescue experiments were used to study the molecular mechanism of CKS1 in colon cancer cells, BALB/c nude mice were used to study the function of CKS1 in vivo. Results CKS1 is highly expressed in colon cancer tissues, and the overexpression of CKS1 promotes cell proliferation and colony formation in both HCT116 (originating from primary colon cancer) and SW620 (originating from metastatic tumor nodules of colon cancer) cells. CKS1-expressing HCT116 cells produced larger tumors than the control cells. The expression pattern of PADI3 and CKS1 are negatively correlation in clinical samples of colon cancer, further study indicates that PADI3 can significantly decrease Hsp90 and CKS1 expression, and Hsp90 is essential for PADI3 to downregulate CKS1expression in colon cancer cells. Conclusions PADI3 exerts its antitumor activity by inhibiting Hsp90 and CKS1 expression, and Hsp90 is essential for PADI3 to suppress CKS1 expression.

scholarly journals Type I, II and X Collagen Gene Expression Pattern in Bone Formation Using rh-BMP2

2005 ◽  
Vol 14 (2) ◽  
pp. 239-240 ◽  
Author(s):  
Naoki Katase ◽  
Hitoshi Nagatsuka ◽  
Yuzo Ishiwari ◽  
Hironobu Konouchi ◽  
Masao Inoue ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Formation ◽  
Expression Pattern ◽  
Gene Expression Pattern ◽  
Type I ◽  
Collagen Gene ◽  
Collagen Gene Expression
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