Activation of the Cap'n'collar C pathway (Nrf2 pathway in vertebrates) signaling in insulin pathway compromised Drosophila melanogaster flies ameliorates the diabetic state upon pro-oxidant conditions.

The insulin pathway is a crucial central system for metabolism and growth. The Nrf2 signaling pathway functions to counteract oxidative stress. Here we sought to study the consequences of an oxidative stress challenge to insulin compromised and control adult flies of different ages, varying the activation state of the Nrf2 pathway in flies, the Cap'n'collar C pathway.

The insulin signaling pathway a century after its discovery: Sexual dimorphism in insulin signaling.

Since practically a century ago, the insulin pathway was discovered in both vertebrates and invertebrates, implying an evolutionarily ancient origin. After a century of research, it is now clear that the insulin signal transduction pathway is a critical, flexible and pleiotropic pathway, evolving into multiple anabolic functions besides glucose homeostasis. It regulates paramount aspects of organismal well-being like growth, longevity, intermediate metabolism, and reproduction.

High glucose concentrations induce oxidative stress by inhibiting Nrf2 expression in rat Müller retinal cells in vitro.

Diabetic retinopathy (DR) is a complication of diabetes. Several studies have implicated oxidative stress as a fundamental factor in the progression of the disease. The nuclear factor erythroid-2-related factor 2 (Nrf2) is one of the main regulators of redox homeostasis.

Retinal Nrf2 expression in normal and early streptozotocin-diabetic rats.

Diabetic retinopathy is the most common cause of vision loss among diabetic patients. Although hyperglycemia produces retinal oxidative stress in long-standing diabetes, the pathogenesis mechanism is unknown. The Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a central role in cell responses against oxidative damage.

Circadian and rhythmic-related behavioral co-morbidities of the diabetic state in Drosophila melanogaster.

Circadian phenomena rule many activities of life on earth. Disruptions in circadian rhythmicity and rhythms have been recognized as a contributing factor for diseased states, for instance metabolic disruptions like diabetes. Diabetes develops as a consequence of faulty insulin pathway signaling, either by lack of insulin production (diabetes type I), or by loss of responsiveness in target tissues (diabetes type 2).

Fos metamorphoses: Lessons from mutants in model organisms.

The Fos oncogene gene family is evolutionarily conserved throughout Eukarya. Fos proteins characteristically have a leucine zipper and a basic region with a helix-turn-helix motif that binds DNA. In vertebrates, there are several Fos homologs.

Development and diabetes on the fly.

We review the use of a model organism to study the effects of a slow course, degenerative disease: namely, diabetes mellitus. Development and aging are biological phenomena entailing reproduction, growth, and differentiation, and then decline and progressive loss of functionality leading ultimately to failure and death. It occurs at all biological levels of organization, from molecular interactions to organismal well being and homeostasis.

acal is a long non-coding RNA in JNK signaling in epithelial shape changes during drosophila dorsal closure.

Dorsal closure is an epithelial remodeling process taking place during Drosophila embryogenesis. JNK signaling coordinates dorsal closure. We identify and characterize acal as a novel negative dorsal closure regulator.

Regulating cell morphogenesis: the Drosophila Jun N-terminal kinase pathway.

The Jun-N-terminal Kinase pathway (JNK), known also as stress activated protein kinase pathway (SAPK), is an eukaryotic evolutionarily conserved signaling pathway. From a purported evolutionarily "ancient" function as stress mediator, it evolved in multicellular eukaryotes to permanent roles in development, without leaving its original function. In Drosophila melanogaster, it is required for follicle cell morphogenesis, embryonic dorsal closure, pupal thoracic closure and genital disc rotation closure, all processes with requisite cell shape changes.

A misexpression study examining dorsal thorax formation in Drosophila melanogaster.

We studied thorax formation in Drosophila melanogaster using a misexpression screen with EP lines and thoracic Gal4 drivers that provide a genetically sensitized background. We identified 191 interacting lines showing alterations of thoracic bristles (number and/or location), thorax and scutellum malformations, lethality, or suppression of the thoracic phenotype used in the screen. We analyzed these lines and showed that known genes with different functional roles (selector, prepattern, proneural, cell cycle regulation, lineage restriction, signaling pathways, transcriptional control, and chromatin organization) are among the modifier lines.