ABSTRACT
Bacillus subtilis under nutritional deprivation exhibits several physiological responses such as synthesis of degradative enzymes, motility, competence, sporulation, etc. At the onset of post-exponential phase the global response regulator, Spo0A, directly or indirectly activates the expression of genes involved in the above processes. These genes are repressed during the exponential phase by a group of proteins called transition state regulators, e.g. AbrB, ScoC and SinR. One such post-exponentially expressed gene is epr, which encodes a minor extracellular serine protease and is involved in the swarming motility of B. subtilis. Deletion studies of the upstream region of epr promoter revealed that epr is co-repressed by transition state regulators, SinR and ScoC. Our study shows that Spo0A positively regulates epr expression by nullifying the repressive effect of co-repressors, SinR and ScoC. We demonstrate via in vitro mobility shift assays that Spo0A binds to the upstream region of epr promoter and in turn occludes the binding site of one of the co-repressor, SinR. This explains the mechanism behind the positive regulatory effect of Spo0A on epr expression.
ABSTRACT
Thyroid hormone resistance (RTH) is inherited as an autosomal dominant trait, with variable clinical presentations. The hallmark of the syndrome is a variable degree of resistance to thyroid hormones, with high levels of circulating thyroid hormones, inappropriately normal or elevated TSH values and a clinical pattern of mixed hypothyroidism and hyperthyroidism. RTH is related in more than 85 percent of cases to thyroid hormone beta receptor mutations. We report a 11 years female with a history of treatment with propylthiouracil (PTU) for hyperthyroidism, presenting with a progressive goiter. Thyroidectomy was performed, removing 233 grams of thyroid tissue showing follicular hyperplasia. After surgery, a fast growth of the remnant thyroid gland was observed along with tachycardia. Laboratory showed a TSH of 38 mU/mL a triiodothyronine level of 300 ng/dL a thyroxin level of 14.8 ug/dL and a free thyroxin of 3.19 ng/dL, suggesting the diagnosis of RTH. The molecular study was negative for mutation of the beta isoform of thyroid hormone receptor. The possible theories that can explain these findings are discussed.
Subject(s)
Humans , Female , Child , Hyperthyroidism/drug therapy , Thyroid Hormone Resistance Syndrome/diagnosis , Thyroxine/administration & dosage , Dose-Response Relationship, Drug , Hyperthyroidism/surgery , Postoperative Period , Thyroid Hormone Resistance Syndrome/etiology , ThyroidectomyABSTRACT
No abstract available.