A5003063598- Neurogenetic and Muscular Disorders Research
- RNA modifications and cancer
- Zebrafish Biomedical Research Applications
- RNA Research and Splicing
- Environmental Toxicology and Ecotoxicology
- Animal Genetics and Reproduction
- Muscle Physiology and Disorders
- Neuroendocrine regulation and behavior
- Neurogenesis and neuroplasticity mechanisms
- Fish Biology and Ecology Studies
- Reproductive biology and impacts on aquatic species
- Maternal Mental Health During Pregnancy and Postpartum
- Stress Responses and Cortisol
- Environmental Science and Water Management
- Neurobiology and Insect Physiology Research
- Axon Guidance and Neuronal Signaling
- Spinal Cord Injury Research
Wittenberg University
2008-2019
The Ohio State University
2005-2009
University of Cologne
2008
Emory University
2008
Institute of Neurobiology and Molecular Medicine
2006
Homozygous deletion of the survival motor neuron 1 gene ( SMN1 ) causes spinal muscular atrophy (SMA), most frequent genetic cause early childhood lethality. In rare instances, however, individuals are asymptomatic despite carrying same mutations as their affected siblings, thereby suggesting influence modifier genes. We discovered that unaffected -deleted females exhibit significantly higher expression plastin 3 PLS3 than SMA-affected counterparts. demonstrated is important for axonogenesis...
Spinal muscular atrophy (SMA) is an autosomal recessive disorder characterized by a loss of α motoneurons in the spinal cord. SMA caused low levels ubiquitously expressed survival motor neuron (Smn) protein. As it unclear how Smn specifically affect motoneurons, we have modeled zebrafish, vertebrate model organism with well-characterized motoneuron development. Using antisense morpholinos to reduce throughout entire embryo, found axon–specific pathfinding defects. Reduction individual...
Spinal muscular atrophy (SMA) is a motor neuron degenerative disease caused by low levels of the survival (SMN) protein and linked to mutations or loss SMN1 retention SMN2 . How SMN cause SMA unclear. functions in small nuclear ribonucleoprotein (snRNP) biogenesis, but recent studies indicate that may also function axons. We showed previously decreasing Smn zebrafish using morpholinos (MO) results axon defects. To determine how outgrowth, we coinjected smn MO with various human RNAs assayed...
Spinal muscular atrophy (SMA), a recessive genetic disease, affects lower motoneurons leading to denervation, atrophy, paralysis and in severe cases death. Reduced levels of survival motor neuron (SMN) protein cause SMA. As first step towards generating model SMA zebrafish, we identified three smn mutations. Two these alleles, smnY262stop smnL265stop , were stop mutations that resulted exon 7 truncation, whereas the third, smnG264D was missense mutation corresponding an amino acid altered...
Abstract A paramount question in spinal muscular atrophy (SMA) research is why reduced levels of SMN, a ubiquitously expressed protein, leads to motoneuron‐specific disease. It has been hypothesized that SMN may have dual function: role snRNP assembly and novel function affects axons. We previously shown decreasing Smn zebrafish causes defects motor axon outgrowth. To determine whether other components the complex would also cause defects, we knocked down Gemin2, binding protein involved...
In the United States, Sevin(™) brand insecticide is one of most commonly used insecticides. The active ingredient in Sevin(™), carbaryl (1-napthyl-N-methylcarbamate), a known acetylcholinesterase (AChE) inhibitor that prevents breakdown acetylcholine to acetate and choline at synapse. While successfully causes death insects by paralysis, it has also been shown have negative effects on development several nontarget species. To study species, zebrafish (Danio rerio) were used, as they are good...