A5023070032- Muscle Physiology and Disorders
- Cardiomyopathy and Myosin Studies
- Cellular Mechanics and Interactions
- Neurobiology and Insect Physiology Research
- Genetics, Aging, and Longevity in Model Organisms
- Nuclear Structure and Function
- Microtubule and mitosis dynamics
- Genetic Neurodegenerative Diseases
- Genetics and Physical Performance
Memorial Sloan Kettering Cancer Center
2019-2024
Sarcomeres, the fundamental contractile units of muscles, are conserved structures composed actin thin filaments and myosin thick filaments. How sarcomeres formed maintained is not well understood. Here, we show that knockdown Drosophila cofilin (DmCFL), an depolymerizing factor, disrupts both sarcomere structure muscle function. The loss DmCFL also results in formation sarcomeric protein aggregates impairs addition during growth. activation proteasome delays deterioration our model....
Cofilin, an actin-severing protein, plays key roles in muscle sarcomere addition and maintenance. Our previous work found that Drosophila cofilin (DmCFL) knockdown causes progressive deterioration of structure function produces features seen nemaline myopathy caused by mutations. We hypothesized disruption actin cytoskeleton dynamics DmCFL would impact other aspects development, and, thus, conducted RNA-sequencing analysis unexpectedly revealed upregulated expression numerous neuromuscular...
Skeletal muscle consists of multinucleated cells in which the myonuclei are evenly spaced throughout cell. In Drosophila, this pattern is established embryonic myotubes, where move via microtubules (MTs) and MT-associated protein Ensconsin (Ens)/MAP7, to achieve their distribution. Ens regulates multiple aspects MT biology, but little known about how itself regulated. We find that physically interacts colocalizes with Bsg25D, Drosophila homologue centrosomal Ninein. Bsg25D loss enhances...
ABSTRACT Proper muscle contraction requires the assembly and maintenance of sarcomeres myofibrils. Although protein components myofibrils are generally known, less is known about mechanisms by which they individually function together synergize for myofibril maintenance. For example, it unclear how disruption actin filament (F-actin) regulatory proteins leads to weakness observed in myopathies. Here, we show that knockdown Drosophila Tropomodulin (Tmod), results several myopathy-related...
Abstract Cofilin, an actin severing protein, plays critical roles in muscle sarcomere addition and maintenance. Our previous work has shown Drosophila cofilin ( DmCFL ) knockdown causes progressive deterioration of structure function produces features seen nemaline myopathy (NM) caused by mutations. We hypothesized that disruption cytoskeleton dynamics would impact other aspects development, and, thus, conducted RNA sequencing analysis which unexpectedly revealed upregulated expression...
SUMMARY Sarcomeres, the fundamental contractile units of muscles, are conserved structures composed actin thin filaments and myosin thick filaments. How sarcomeres formed maintained is not well understood. Here, we show that knockdown Drosophila Cofilin ( DmCFL) , an depolymerizing factor, leads to progressive disruption sarcomere structure muscle function in vivo . Loss DmCFL also results formation sarcomeric protein aggregates impairs addition during growth. Strikingly, activation...
Sarcomeres, the fundamental contractile units of muscles, are conserved structures composed actin thin filaments and myosin thick filaments. How sarcomeres formed maintained is not well understood. Here we show that knockdown Drosophila Cofilin (DmCFL), an depolymerizing factor, disrupts both sarcomere structure muscle function. Loss DmCFL also results in formation sarcomeric protein aggregates impairs addition during growth. Strikingly, activation proteasome delays deterioration our model....
ABSTRACT Proper muscle contraction requires the assembly and maintenance of sarcomeres myofibrils. While protein components myofibrils are generally known, less is known about mechanisms by which they individually function together synergize for myofibril maintenance. For example, it unclear how disruption actin filament (F-actin) regulatory proteins leads to weakness observed in myopathies. Here, we show that knockdown Drosophila Tropomodulin (Tmod) results several myopathy-related...