Zhu H, Han M. Exploring developmental and physiological functions of fatty acid and lipid variants through worm and fly genetics. Annu Rev Genet. 2014;48:119-48. PMID: 25195508.
From the abstract: "Lipids are more than biomolecules for energy storage and membrane structure. With ample structural variation, lipids critically participate in nearly all aspects of cellular function. Lipid homeostasis and metabolism are closely related to major human diseases and health problems. However, lipid functional studies have been significantly underdeveloped ... Here, we review a subset of these studies using Caenorhabditis elegans and Drosophila melanogaster."
Saturday, July 11, 2015
Review--Drosophila as a model for study of sleep disorders
Donelson NC, Sanyal S. Use of Drosophila in the investigation of Sleep Disorders. Exp Neurol. 2015 Jul 6. pii: S0014-4886(15)30034-0. PMID: 26160555.
From the abstract: "Genetic underpinnings for sleep disorders in humans remain poorly identified, investigated and understood. ... On the other hand, there have been steady and remarkable developments in the investigation of sleep using model organisms such as Drosophila. ... Here, we discuss the opportunities and limitations of studying sleep disorders in Drosophila and propose that a greater convergence of basic sleep research in model organisms and human genetics should catalyze better understanding of sleep disorders and generate viable therapeutic options."
From the abstract: "Genetic underpinnings for sleep disorders in humans remain poorly identified, investigated and understood. ... On the other hand, there have been steady and remarkable developments in the investigation of sleep using model organisms such as Drosophila. ... Here, we discuss the opportunities and limitations of studying sleep disorders in Drosophila and propose that a greater convergence of basic sleep research in model organisms and human genetics should catalyze better understanding of sleep disorders and generate viable therapeutic options."
Friday, July 10, 2015
Fly model points to possible new target pathway for treatment of Friedreich’s ataxia
Pablo Calap-Quintana, Sirena Soriano, José Vicente Llorens, Ismael Al-Ramahi, Juan Botas, María Dolores Moltó, María José Martínez-Sebastián. TORC1 Inhibition by Rapamycin Promotes Antioxidant Defences in a Drosophila Model of Friedreich’s Ataxia. PLOS Published: July 9, 2015 DOI: 10.1371/journal.pone.0132376
From the abstract: "Friedreich’s ataxia (FRDA) ... is a multisystemic disease caused by a significant decrease in the frataxin level. ... we performed a candidate genetic screen in a Drosophila RNAi-based model of FRDA. We found that genetic reduction in TOR Complex 1 (TORC1) signalling improves the impaired motor performance phenotype of FRDA model flies. ... These results point to the TORC1 pathway as a new potential therapeutic target for FRDA and as a guide to finding new promising molecules for disease treatment."
From the abstract: "Friedreich’s ataxia (FRDA) ... is a multisystemic disease caused by a significant decrease in the frataxin level. ... we performed a candidate genetic screen in a Drosophila RNAi-based model of FRDA. We found that genetic reduction in TOR Complex 1 (TORC1) signalling improves the impaired motor performance phenotype of FRDA model flies. ... These results point to the TORC1 pathway as a new potential therapeutic target for FRDA and as a guide to finding new promising molecules for disease treatment."
Suppression of TDP-43 toxicity by newly identified factor in fly models of ALS
Chou CC, Alexeeva OM, Yamada S, Pribadi A, Zhang Y, Mo B, Williams KR, Zarnescu DC, Rossoll W. PABPN1 suppresses TDP-43 toxicity in ALS disease models. Hum Mol Genet. 2015 Jun 30. pii: ddv238. PMID: 26130692.
From the abstract: "TAR DNA-binding protein 43 (TDP-43) is a major disease protein in amyotrophic lateral sclerosis (ALS) and related neurodegenerative diseases. Both the cytoplasmic accumulation of toxic ubiquitinated and hyperphosphorylated TDP-43 fragments and the loss of normal TDP-43 from the nucleus may contribute to the disease progression by impairing normal RNA and protein homeostasis. Therefore, both the removal of pathological protein and the rescue of TDP-43 mislocalization may be critical for halting or reversing TDP-43 proteinopathies. Here, we report poly(A)-binding protein nuclear 1 (PABPN1) as a novel TDP-43 interaction partner that acts as a potent suppressor of TDP-43 toxicity. ... These findings demonstrate a role for PABPN1 in rescuing several cytopathological features of TDP-43 proteinopathy by increasing the turnover of pathologic proteins."
From the abstract: "TAR DNA-binding protein 43 (TDP-43) is a major disease protein in amyotrophic lateral sclerosis (ALS) and related neurodegenerative diseases. Both the cytoplasmic accumulation of toxic ubiquitinated and hyperphosphorylated TDP-43 fragments and the loss of normal TDP-43 from the nucleus may contribute to the disease progression by impairing normal RNA and protein homeostasis. Therefore, both the removal of pathological protein and the rescue of TDP-43 mislocalization may be critical for halting or reversing TDP-43 proteinopathies. Here, we report poly(A)-binding protein nuclear 1 (PABPN1) as a novel TDP-43 interaction partner that acts as a potent suppressor of TDP-43 toxicity. ... These findings demonstrate a role for PABPN1 in rescuing several cytopathological features of TDP-43 proteinopathy by increasing the turnover of pathologic proteins."
Quantifying climbing defects in fly models of neurodegeneration--protocol video
Madabattula ST, Strautman JC, Bysice AM, O'Sullivan JA, Androschuk A, Rosenfelt C, Doucet K, Rouleau G, Bolduc F. Quantitative Analysis of Climbing Defects in a Drosophila Model of Neurodegenerative Disorders. J Vis Exp. 2015 Jun 13;(100). PMID: 26132637.
From the abstract: "... The assay is performed in a glass graduated cylinder, which is sealed with a wax barrier film. By increasing the threshold distance to be climbed to 17.5 cm and increasing the experiment duration to 2 min we have observed a greater sensitivity in detecting mild mobility dysfunctions. ..."
From the abstract: "... The assay is performed in a glass graduated cylinder, which is sealed with a wax barrier film. By increasing the threshold distance to be climbed to 17.5 cm and increasing the experiment duration to 2 min we have observed a greater sensitivity in detecting mild mobility dysfunctions. ..."
New fly model of obesity-related heart disease
Hardy CM, Birse RT, Wolf MJ, Yu L, Bodmer R, Gibbs AG. Obesity-associated Cardiac Dysfunction in Starvation-Selected Drosophila melanogaster. Am J Physiol Regul Integr Comp Physiol. 2015 Jul 1:ajpregu.00160.2015. PMID: 26136533.
Translation in fly models of CMT neuropathy
Niehues S, Bussmann J, Steffes G, Erdmann I, Köhrer C, Sun L, Wagner M, Schäfer K, Wang G, Koerdt SN, Stum M, RajBhandary UL, Thomas U, Aberle H, Burgess RW, Yang XL, Dieterich D, Storkebaum E. Impaired protein translation in Drosophila models for Charcot-Marie-Tooth neuropathy caused by mutant tRNA synthetases. Nat Commun. 2015 Jul 3;6:7520. PMID: 26138142.
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