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The fruit fly, Drosophila melanogaster (Meigen, 1830) has been established as a key model organism thanks in part to their considerable biological similarity to mammals and an abundance of available genetic tools. Drosophila have been used to model many human disease states and have been critical in elucidating the genetic mechanisms contributing to them. Part I of this chapter covered basic Drosophila biology and relevant genetic tools available to Drosophila researchers. Here in part II, we review the use of Drosophila as a model organism to study neurodegenerative disorders, cardiovascular diseases, kidney diseases, cancer, metabolic disorders, and immune disorders, as well as key findings made in those fields thanks to Drosophila research.
This book contains 12 chapters divided into two sections. Section 1 is "Drosophila - Model for Genetics." It covers introduction, chromosomal polymorphism, polytene chromosomes, chromosomal inversion, chromosomal evolution, cell cycle regulators in meiosis and nongenetic transgenerational inheritance in Drosophila. It also includes ecological genetics, wild-type strains, morphometric analysis, cytostatics, frequencies of early and late embryonic lethals (EEL and LEL) and mosaic imaginal discs of Drosophila for genetic analysis in biomedical research. Section 2 is "Drosophila - Model for Therapeutics." It explains Drosophila as model for human diseases, neurodegeneration, heart-kidney metabolic disorders, cancer, pathophysiology of Parkinson's disease, dopamine, neuroprotective therapeutics, mitochondrial dysfunction and translational research. It also covers Drosophila role in ubiquitin-carboxyl-terminal hydrolase-L1 (UCH-L1) protein, eye development, anti-dUCH antibody, neuropathy target esterase (NTE), organophosphorous compound-induced delayed neuropathy (OPIDN) and hereditary spastic paraplegia (HSP). It also includes substrate specificities, kinetic parameters of recombinant glutathione S-transferases E6 and E7 (DmGSTE6 and DmGSTE7), detoxification and insecticidal resistance and antiviral immunity in Drosophila.
Most biological pathways, physical and neurological properties are highly conserved between humans and Drosophila and nearly 75% of human disease-causing genes have a functional homologue in Drosophila. This volume provides recent advances in Drosophila models for various human diseases, with each chapter providing a review of studies involving Drosophila models, as well as detailed protocols commonly used in laboratories. Starting with a review of Drosophila’s value as a highly tractable model organism for studying human diseases, subsequent chapters present Drosophila models for specific human diseases. The book provides a useful resource for all scientists who are starting to use the Drosophila model in their studies, and for researchers working in the pharmaceutical industry and using new screening models to develop new medicines for various diseases.
The fruit fly, Drosophila melanogaster (Meigen, 1830) has been established as a cornerstone for research into a wide array of subjects including diseases, development, physiology, and genetics. Thanks to an abundance of genetic tools, publicly available fly stocks, and databases, as well as their considerable biological similarity to mammalian systems, Drosophila has been solidified as a key model organism for elucidating many aspects of human disease. Herein is presented an overview of what makes Drosophila such an appealing model organism. In Part I of this chapter, basic Drosophila biology is reviewed and the most relevant genetic tools available to Drosophila researchers are covered. Then in part II, we outline the use of Drosophila as a model organism to study a wide array of pathologies in which Drosophila has been used, along with key advances made in the specific field using the fly as a model organism.
A single species of fly, Drosophila melanogaster, has been the subject of scientific research for more than one hundred years. Why does this tiny insect merit such intense scrutiny? Drosophila’s importance as a research organism began with its short life cycle, ability to reproduce in large numbers, and easy-to-see mutant phenotypes. Over time, laboratory investigation revealed surprising similarities between flies and other animals at the level of genes, gene networks, cell interactions, physiology, immunity, and behavior. Like humans, flies learn and remember, fight microbial infection, and slow down as they age. Scientists use Drosophila to investigate complex biological activities in a simple but intact living system. Fly research provides answers to some of the most challenging questions in biology and biomedicine, including how cells transmit signals and form ordered structures, how we can interpret the wealth of human genome data now available, and how we can develop effective treatments for cancer, diabetes, and neurodegenerative diseases. Written by a leader in the Drosophila research community, First in Fly celebrates key insights uncovered by investigators using this model organism. Stephanie Elizabeth Mohr draws on these “first in fly” findings to introduce fundamental biological concepts gained over the last century and explore how research in the common fruit fly has expanded our understanding of human health and disease.
Motor neuron diseases are the most catastrophic of neurodegenerative disorders. The cognitive function is spared, but the motor neuron degeneration translates into progressive muscle weakness and paralysis that propel the afflicted patient to eventual death. Neurodegenerative disorders constitute one of the major challenges of modern medicine in view of the current lack of effective therapies. The fruit fly, Drosophila melanogaster, has a distinguished history as an important model organism capable of shaping our fundamental understanding of life. Remarkably, the vast majority of all known human disease genes have a similar fly counterpart and at the molecular and physiological level, the basic principles of neuromuscular function are amazingly conserved between humans and Drosophila. Combine this with the presence of numerous genetic tools developed over the last century allowing genes and the proteins they encode to be manipulated swiftly to decipher their in vivo function and you have a superb genetic animal model organism of disease.This publication singles out the past and recent accomplishments of Drosophila in modelling motor neuron disease including amyotrophic lateral sclerosis (Lou Gehrigs disease), hereditary spastic paraplegias, Charcot-Marie-Tooth disease, spinal and bulbar muscular atrophy (Kennedys disease) and spinal muscular atrophy. The emphasis is on recent developments including the emerging molecular pathways underpinning these disorders. Genetic screens aimed at identifying novel genes that cause motor neuron degeneration or finding modifiers of the phenotype resulting from the disruption of disease-causative genes are also tackled. Importantly, this collection provides an inspiring look at the indispensability of the fruit fly, and of model organisms in general, to neuroscience research.
This volume provides a series of review articles that capture the advances in using the fruit fly, Drosophila melanogaster, model system to address a wide range of cancer-related topics. Articles in this book provide case studies that shed light on the intricate cellular and molecular mechanisms underlying tumor formation and progression. Readers will discover the beauty of the fly model’s genetic simplicity and the vast arsenal of powerful genetic tools enabling its efficient and adaptable use. This model organism has provided a unique opportunity to address questions regarding cancer initiation and development that would be extremely challenging in other model systems. This book provides a useful resource for a researcher who wishes to learn about and apply the Drosophila model to tackle fundamental questions in cancer biology, and to find new ways to fight against this devastating disease.
Scientific Frontiers in Developmental Toxicology and Risk Assessment reviews advances made during the last 10-15 years in fields such as developmental biology, molecular biology, and genetics. It describes a novel approach for how these advances might be used in combination with existing methodologies to further the understanding of mechanisms of developmental toxicity, to improve the assessment of chemicals for their ability to cause developmental toxicity, and to improve risk assessment for developmental defects. For example, based on the recent advances, even the smallest, simplest laboratory animals such as the fruit fly, roundworm, and zebrafish might be able to serve as developmental toxicological models for human biological systems. Use of such organisms might allow for rapid and inexpensive testing of large numbers of chemicals for their potential to cause developmental toxicity; presently, there are little or no developmental toxicity data available for the majority of natural and manufactured chemicals in use. This new approach to developmental toxicology and risk assessment will require simultaneous research on several fronts by experts from multiple scientific disciplines, including developmental toxicologists, developmental biologists, geneticists, epidemiologists, and biostatisticians.
This book is aimed at generating an updated reservoir of scientific endeavors undertaken to unravel the complicated yet intriguing topic of neurodegeneration. Scientists from Europe, USA and India who are experts in the field of neurodegenerative diseases have contributed to this book. This book will help readers gain insight into the recent knowledge obtained from Drosophila model, in understanding the molecular mechanisms underlying neurodegenerative disorders and also unravel novel scopes for therapeutic interventions. Different methodologies available to create humanized fly models that faithfully reflects the pathogenicities associated with particular disorders have been described here. It also includes information on the exciting area of neural stem cells. A brief discussion on neurofibrillary tangles, precedes the elaborate description of lessons learnt from Drosophila about Alzheimer's, Parkinson’s, Spinomuscular Atrophy, Huntington’s diseases, RNA expansion disorders and Hereditary Spastic Paraplegia. We have concluded the book with the use of Drosophila for identifying pharmacological therapies for neurodegenerative disorders. The wide range of topics covered here will not only be relevant for beginners who are new to the concept of the extensive utility of Drosophila as a model to study human disorders; but will also be an important contribution to the scientific community, with an insight into the paradigm shift in our understanding of neurodegenerative disorders. Completed with informative tables and communicative illustrations this book will keep the readers glued and intrigued. We have comprehensively anthologized the lessons learnt on neurodegeneration from Drosophila and have thus provided an insight into the multidimensional aspects of pathogenicities of majority of the neurodegenerative disorders.
Epigenetic Mechanisms of the Cambrian Explosion provides readers with a basic biological knowledge and epigenetic explanation of the biological puzzle of the Cambrian explosion, the unprecedented rapid diversification of animals that began 542 million years ago. During an evolutionarily instant of ~10 million years, which represents only 0.3% of the time of existence of life on Earth, or less than 2% of the time of existence of metazoans, all of the 30 extant body plans, major animal groups (phyla) and several extinct groups appeared. The work helps address this phenomena and tries to answer remaining questions for evolutionary biology, epigenetics, and scientific researchers. The book recognizes and presents objective representations of alternative theories for epigenetic evolution in this period, with the author drawing on his epigenetic theory of evolution to explain the causal basis of the Cambrian explosion. Both empirical evidence and theoretical arguments are presented in support of this thought-provoking epigenetic theory. Explains the Cambrian explosion from an entirely epigenetic view Takes a causal rather than descriptive approach to the phenomenon Allows for a broad readership, including those with only a basic biological knowledge, while maintaining scientific rigor