Syndicate content

Archive - Mar 10, 2017

Scientists Study Genetics Underlying Novel Egg-Laying Behavior of Fruit Fly Species That Causes Enormous Damage to Soft-Fruit Crops

In contrast to other members of the Drosophila family, the spotted-wing fly D. suzukii deposits its eggs in ripe fruits. Biologists from Ludwig-Maximilians-Universitaet (LMU) in Munich, Germany, have now elucidated the sensory basis of D. suzukii’s ability to exploit a novel ecological niche. Unlike most species of the genus Drosophila, which deposit their eggs in fermenting fruits, D. suzukii lays its eggs in ripe fruits. This apparently minor difference in behavior can have catastrophic consequences for commercial fruit-growers, and has made the species into a crop pest--for the puncture made by the female's ovipositor facilitates infections, while the hatched larvae feed on the fruit pulp. As a result, these infestations cause enormous damage to soft-fruit crops, such as cherries, raspberries, grapes, and strawberries. LMU biologists led by Professor Nicolas Gompel, in a collaboration with the groups of Dr. Benjamin Prud'homme (CNRS, France) and Professor Ilona Grunwald Kadow (Technical University, Munich), have begun to explore the genetic basis for this unusual egg-laying behavior. Their findings were published online on March 9, 2017 in Current Biology. The article is titled “Evolution of Multiple Sensory Systems Drives Novel Egg-Laying Behavior in the Fruit Pest Drosophila suzukii.” The researchers combined behavioral tests and genetic methods to determine how the closely related Drosophilid species D. melanogaster, D. biarmipes, and D. suzukii go about choosing the ideal nursery for their brood, each in their own way. The experiments showed that, in the search for egg-laying sites, the flies respond to the texture of the fruit, to the chemical composition of the surface and to characteristic odor compounds. In other words, they use the senses of smell, touch, and taste. D.

Researchers Find a Gene That Causes Very Rare Opitz C Syndrome

Opitz C syndrome is an extremely rare genetic disease that causes severe disabilities in patients and has been diagnosed in three people in the Iberian Peninsula, and sixty people in the world. A team led by the Professors Daniel Grinberg and Susana Balcells, from the Group on Human Molecular Genetics of the University of Barcelona and the Biomedical Research Networking Center of Rare Diseases (CIBERER) has now identified a gene that causes the Opitz C syndrome in the only patient in Catalonia, Spain, diagnosed with this severe congenital disease. This new scientific advance is a first step to discover the genetic bases of this syndrome which, so far, does not offer treatment possibilities, prenatal diagnosis, or genetic counseling. The new study, published online on March 10, 2017 in the journal Scientific Reports, has the participation of several researchers at the CRG, including members of the Genomic and Epigenomic Variation in Disease laboratory, the Genomics Unit, and the Bioinformatics Unit. It also had the participation of John M. Opitz (University of Utah, United States), Giovanni Neri (Catholic University of the Sacred Heart, Italy) and experts at the Department of Clinical and Molecular Genetics of the University Hospital Vall d'Hebron (VHIR). The open-access article is titled “A De Novo Nonsense Mutation in MAGEL2 in a Patient Initially Diagnosed As Opitz-C: Similarities Between Schaaf-Yang and Opitz-C Syndromes.” The genetic bases of this very rare disease, described for the first time in 1969 by Dr. John M. Opitz, are still unknown. It is generally thought that its origin can be traced to the occurrence of dominant, maternally silenced de novo mutations.

Fungal Protein Stimulates Axon Regeneration Via 14-3-3 Protein-Protein Stabilization; Work Identifies Possible Targets of Future Drug Development for Spinal Cord Injury & Stroke

A foray into plant biology has led one researcher to discover that a natural molecule can stimulate the repair of axons, the thread-like projections that carry electrical signals between neurons. Axonal damage is the major culprit underlying disability in conditions such as spinal cord injury and stroke. Andrew Kaplan, a Ph.D. candidate at the Montreal Neurological Institute and Hospital of McGill University in Canada, was looking for a pharmacological approach to axon regeneration, with a focus on 14-3-3, a family of proteins with neuroprotective functions that have been under investigation in the laboratory of Dr. Alyson Fournier, Professor of Neurology and Neurosurgery and senior author on the study. During Kaplan’s search, he found research describing how plants respond to a specific type of fungal infection. When plants are exposed to fusicoccin-A, a small molecule produced by a certain strain of fungus, the leaves of the plant wilt, but the roots grow longer. Fusicoccin-A affects 14-3-3 activity by stabilizing its interactions with other proteins. "While 14-3-3 is the common denominator in this phenomenon, the identity of the other proteins involved and the resulting biological activities differ between plants and animals," says Kaplan. He theorized that fusicoccin-A could be an effective way of harnessing 14-3-3 to repair axons. To test this theory, he and his fellow researchers treated mechanically damaged neurons in culture with the molecule and observed the results. "When I looked under the microscope the following day, the axons were growing like weeds, an exciting result that led us to determine that fusicoccin-A can stimulate axon repair in the injured nervous system," says Kaplan. The new work was published online on March 8, 2017 in Neuron.