The intestinal epithelium has a high cell turnover rate and is an excellent system to study stem cell-mediated adaptive growth. Ingestion of food particles regulates the mechanosensing Misshapen-Yorkie pathway in Drosophila intestinal growth. J., Ostroff, G., Mao, J., Wang, Q., Xu, L. Altering the levels or localization of Msn also led to changes in the actin cytoskeleton and altered the localization of E-cadherin, which suggests that Msn could be indirectly limiting ring canal size by altering the structure or dynamics of the actin cytoskeleton and/or adherens junctions. Over-expression of Msn decreased ring canal diameter, and expression of a membrane tethered form of Msn caused ring canal detachment and nurse cell fusion. Msn localizes to ring canals throughout most of oogenesis, and depletion of Msn led to the formation of larger ring canals. This study demonstrates a novel role for the Ste20 family kinase, Misshapen (Msn), in regulation of the size of the germline ring canals. The ring canals are enriched in actin and actin binding proteins, and many proteins have been identified that localize to the germline ring canals and control their expansion and stability.
Within the developing egg chamber, the germ cells (15 nurse cells and 1 oocyte) are connected to each other through intercellular bridges called ring canals, which expand over the course of oogenesis to support the transfer of materials from the nurse cells to the oocyte. This study used the Drosophila egg chamber to study the mechanisms that regulate intercellular bridges. Intercellular bridges are conserved structures that allow neighboring cells to exchange cytoplasmic material defects in intercellular bridges can lead to infertility in many organisms. The Misshapen kinase regulates the size and stability of the germline ring canals in the Drosophila egg chamber. Thus, this study provides a yet unknown mode of regulation of Leads to accumulation of membrane-tethered form of Notch. It was further shown that kinase active Misshapen KinaseĪctive form of Msn associates with Notch receptor and regulates its Genetically interacts with components of Notch signaling pathway. Phenotypes similar to Notch loss-of-function condition and msn Overexpression of kinase active form of Msn exhibits Signaling, this study identified msn as a novel regulator of In a genetic screen, usingĬandidate gene approach to identify novel kinases involved in Notch Yeast Ste20p (sterile 20 protein) kinase. ( msn) encodes a protein kinase, which is related to the budding Principal cellular communication system that plays a pivotal role duringĭevelopment of metazoans. andĪctive Misshapen regulates Notch signaling in Drosophila Subchondral bone sclerosis and bone marrow lesions can occur at any time but are particularly common in the later stages of knee arthritis.Keywords - dorsal closure, JNK pathway, Sterile 20 MAP kinase kinase kinaseĬellular location - presumably cytoplasmic These lesions may be associated with knee pain. The bone underneath damaged or missing knee cartilage may develop cysts (typically referred to as “subchondral cysts”) and areas of abnormal swelling called bone marrow lesions. (“Chondral” means cartilage subchondral bone is located just beneath cartilage. The surfaces of the tibia and femur that lie just beneath knee cartilage can change in composition and harden. It is important to note that bone spurs are a normal sign of aging, and the presence of them alone is not a cause for concern. The bone spurs can create more friction in the knee joint, leading to discomfort and pain. It is believed that bones produce bone spurs to compensate for deteriorated or missing cartilage by redistributing weight loads. Abnormal bony growths, called osteophytes or bone spurs, develop on the bone at the knee joint. This can cause the bone to undergo changes. When cartilage is damaged, bones experience more friction and impact.