scholarly journals Nitric Oxide Synthase Mediates Growth Coordination During Drosophila Melanogaster Imaginal Disc Regeneration

2015 ◽  
Author(s):  
Jacob Jaszczak
Keyword(s):  
Nitric Oxide ◽  
Drosophila Melanogaster ◽  
Nitric Oxide Synthase ◽  
Imaginal Disc ◽  
Disc Regeneration ◽  
Oxide Synthase

scholarly journals Relations between nitric oxide synthase DNOS1, Hsp70 and apoptosis regulatory gene grim in Drosophila melanogaster after heat stress induction

2010 ◽  
Vol 26 (3) ◽  
pp. 194-199
Author(s):  
E. M. Khussainova ◽  
Z. A. Bulentayeva ◽  
B. O. Bekmanov ◽  
L. B. Djansugurova ◽  
R. I. Bersimbayev
Keyword(s):  
Nitric Oxide ◽  
Drosophila Melanogaster ◽  
Heat Stress ◽  
Nitric Oxide Synthase ◽  
Regulatory Gene ◽  
Stress Induction ◽  
Oxide Synthase

scholarly journals The relaxin receptor Lgr3 mediates growth coordination and developmental delay during Drosophila melanogaster imaginal disc regeneration

2015 ◽  
Author(s):  
Jacob S. Jaszczak ◽  
Jacob B. Wolpe ◽  
Rajan Bhandari ◽  
Rebecca G. Jaszczak ◽  
Adrian Halme
Keyword(s):  
Drosophila Melanogaster ◽  
Developmental Delay ◽  
Imaginal Disc ◽  
Imaginal Discs ◽  
Prothoracic Gland ◽  
Disc Regeneration ◽  
Relaxin Family ◽  
Dependent Growth ◽  
Oxide Synthase ◽  
Relaxin Receptor

Damage to Drosophila melanogaster imaginal discs activates a regeneration checkpoint that 1) extends larval development and 2) coordinates the regeneration of the damaged disc with the growth of undamaged discs. These two systemic responses to damage are both mediated by Dilp8, a member of the insulin/IGF/relaxin family of peptide hormones, which is released by regenerating imaginal discs. Growth coordination between regenerating and undamaged imaginal discs is dependent on Dilp8 activation of NOS in the prothoracic gland (PG), which slows the growth of undamaged discs by limiting ecdysone synthesis. Here we demonstrate that the Drosophila relaxin receptor homologue Lgr3, a leucine-rich repeat-containing G-protein coupled receptor, is required for Dilp8-dependent growth coordination and developmental delay during the regeneration checkpoint. Lgr3 regulates these responses to damage via distinct mechanisms in different tissues. Using tissue-specific RNAi disruption of Lgr3 expression, we show that Lgr3 functions in the PG upstream of nitric oxide synthase (NOS), and is necessary for NOS activation and growth coordination during the regeneration checkpoint. When Lgr3 is depleted from neurons, imaginal disc damage no longer produces either developmental delay or growth inhibition. To reconcile these discrete tissue requirements for Lgr3 during regenerative growth coordination, we demonstrate that Lgr3 activity in the both the CNS and PG is necessary for NOS activation in the PG following damage. Together, these results identify new roles for a relaxin receptor in mediating damage signaling to regulate growth and developmental timing.

scholarly journals Nitric Oxide Synthase Regulates Growth Coordination DuringDrosophila melanogasterImaginal Disc Regeneration

Genetics ◽  
2015 ◽  
Vol 200 (4) ◽  
pp. 1219-1228 ◽  
Author(s):  
Jacob S. Jaszczak ◽  
Jacob B. Wolpe ◽  
Anh Q. Dao ◽  
Adrian Halme
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Disc Regeneration ◽  
Oxide Synthase

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric oxide synthase and cellac disease

2001 ◽  
Vol 120 (5) ◽  
pp. A684-A684
Author(s):  
I DANIELS ◽  
I MURRAY ◽  
W GODDARD ◽  
R LONG
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase
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