Subject(s)
Clinical Trials as Topic , Glucagon-Like Peptides , Kidney Diseases , Humans , Kidney Diseases/drug therapy , Kidney Diseases/etiology , Kidney Diseases/mortality , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/mortality , Glucagon-Like Peptides/therapeutic useSubject(s)
Clinical Trials as Topic , Exercise Therapy , National Institutes of Health (U.S.) , Post-Acute COVID-19 Syndrome , Research Support as Topic , Humans , National Institutes of Health (U.S.)/economics , National Institutes of Health (U.S.)/organization & administration , Post-Acute COVID-19 Syndrome/therapy , Research Support as Topic/methods , Research Support as Topic/organization & administration , United States , Exercise Therapy/adverse effectsABSTRACT
In C. elegans, the Sma/Mab TGFbeta signaling pathway regulates body size and male tail patterning. SMA-9, the C. elegans homolog of Schnurri, has been shown to function as a downstream component to mediate the Sma/Mab TGFbeta signaling pathway in these processes. We have discovered a new role for SMA-9 in dorsoventral patterning of the C. elegans post-embryonic mesoderm, the M lineage. In addition to a small body size, sma-9 mutant animals exhibit a dorsal-to-ventral fate transformation within the M lineage. This M lineage defect of sma-9 mutants is unique in that animals carrying mutations in all other known components of the TGFbeta pathway exhibit no M lineage defects. Surprisingly, mutations in the core components of the Sma/Mab TGFbeta signaling pathway suppressed the M lineage defects of sma-9 mutants without suppressing their body size defects. We show that this suppression specifically happens within the M lineage. Our studies have uncovered an unexpected role of SMA-9 in antagonizing the TGFbeta signaling pathway during mesodermal patterning, suggesting a novel mode of function for the SMA-9/Schnurri family of proteins.
