AT A GLANCE
- Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity
Summary: This at a glance article gives an overview of the recent knowledge mainly derived from rodent models regarding the CNS-dependent regulation of energy and glucose homeostasis, and depicts how dysregulation of the involved neuronal networks promotes overnutrition and obesity.
REVIEW
- Induced pluripotent stem cell models of lysosomal storage disorders
Summary: This Review discusses how induced pluripotent stem cells (iPSCs) provide new opportunities to explore the biology and pathophysiology of lysosomal storage diseases, and how iPSCs have illuminated the role of lysosomes in more common disorders.
RESEARCH ARTICLES
- SlgA, encoded by the homolog of the human schizophrenia-associated gene PRODH, acts in clock neurons to regulate Drosophila aggression
Editors' choice: A Drosophila model to study the role of PRODH, a schizophrenia-associated gene, in behavioral disorders.
- Dietary reversal of neuropathy in a murine model of prediabetes and metabolic syndrome
Summary: A mouse model of metabolic syndrome can be used to investigate peripheral nerve damage, enabling the development of mechanism-based therapies for neuropathy.
- Paneth-cell-disruption-induced necrotizing enterocolitis in mice requires live bacteria and occurs independently of TLR4 signaling
Summary: Paneth cell disruption and bacterial exposure in immature murine intestine induces NEC-like pathology. Importantly, this occurs independently of TLR4 activation, presenting an alternative mechanism for disease development.
- Characterization of Drosophila Saposin-related mutants as a model for lysosomal sphingolipid storage diseases
Summary: Detailed analysis of lipid accumulation, lysosomal dysfunction and neurodegeneration in a Drosophila sphingolipidosis model, suitable for studying the resulting pathological signaling events.
- Upregulation of distinct collagen transcripts in post-surgery scar tissue: a study of conjunctival fibrosis
Summary: As well as providing an objective quantitative measure, distinct collagen genes may further aid in the characterization and definition of the development of fibrosis.
- A Drosophila model of dominant inclusion body myopathy type 3 shows diminished myosin kinetics that reduce muscle power and yield myofibrillar defects
Summary: Reduced muscle power output and progressive myofibrillar defects in a Drosophila model of inclusion body myopathy 3 arise from the decreased rate of weak to strong actin-binding transition of myosin.
- A mouse model for inherited renal fibrosis associated with endoplasmic reticulum stress
Summary: A mouse model for renal fibrosis caused by uromodulin mutations reveals roles for ER stress and the unfolded protein response.
- Progesterone induces neuroprotection following reperfusion-promoted mitochondrial dysfunction after focal cerebral ischemia in rats
Summary: Progesterone treatment is beneficial in preserving the altered mitochondrial functions in cerebral ischemic injury and thus can help in defining better therapies.
RESOURCE ARTICLES
- A classification system for zebrafish adipose tissues
Summary: A standardized nomenclature and classification system for zebrafish adipose tissues and regression models to predict expected adipose size during the course of zebrafish development.
- A rapid and effective method for screening, sequencing and reporter verification of engineered frameshift mutations in zebrafish
Summary: A new CRISPR/Cas9-based method of fluorescent reporter technology in zebrafish to confirm loss of gene function in this model.
This issue
Other journals from The Company of Biologists
Editor’s choice - Enhancer of Polycomb and the Tip60 complex repress hematological tumor initiation by negatively regulating JAK/STAT pathway activity
Using Drosophila as a low-complexity model for human myeloproliferative neoplasms, Erika Bach and team identified a conserved mechanism by which the Tip60 lysine acetyltransferase acts as a tumor suppressor by repressing JAK protein expression in a histone-independent manner.
This Review summarizes some of the exciting work that has used Drosophila as a model for the ever-expanding field of intellectual disability and autism spectrum disorders. Annette Schenck and team highlight disease-relevant assays, emerging themes and future challenges.
The beneficial effects of exercise against diet-induced early obesity and NAFLD are mediated by its capacity to modulate intestinal microbiota composition and functionality, restore lipid metabolism and prevent disruption of the gut-liver axis, show Sonia Sánchez-Campos and colleagues.
First Person interviews
Have you seen our interviews with the early-career first authors of our papers? Recently, we caught up with Susan Motch Perrine and Meng Wu, Alessandro Bailetti, Tuba Sural-Fehr and Scott Collum.
Don't miss your chance to attend our DMM Journal Meeting in Boston. Deadline to apply is 21 June 2019. Join organisers Monica Justice, Nancy Speck, Paresh Vyas and Leonard Zon.
Call for papers – A guide to using neuromuscular disease models for basic and preclinical studies
We invite you to submit original research for a Special Collection focused on neuromuscular disease models, edited by Annemieke Aartsma-Rus, James Dowling and Maaike van Putten. The collection will showcase studies on the dysregulation of pathways, disease progression, approaches to treat and modify disease course in animal models, technologies for studying muscle pathophysiology and regeneration, and advances in the development of suitable in vitro and in vivo models. Deadline extended to 1 July 2019.
Meet the preLighters: an interview with Tessa Sinnige
Tessa Sinnige is a postdoctoral fellow who recently moved to Northwestern University, USA from the University of Cambridge. In her research she studies the mechanisms of protein aggregation using C. elegans as a model. We caught up with Tessa to discuss about her science, postdoc life, preprints and her experience with preLights.
Catch up with recent preLights selected for the translational biology community.