To identify the structural defects of nonsporulating mutants of Streptomyces griseus, the wild-type strain and class III bald mutants were examined by using transmission electron microscopy, ultrasonic treatment, and fluorescence microscopy after the induction of submerged sporulation by phosphate starvation. In the wild-type strain, submerged sporulation was marked by the relatively synchronous formation of sporogenic hyphae, nucleoid segregation, deposition of sporulation septa, and subsequent thickening of the spore walls during maturation. All of the class III mutants prematurely synthesized sporulation septa and thick spore walls. The class IIIA and C mutants formed sporogenic hyphae earlier than the wild-type strain and underwent nucleoid segregation in parallel with sporulation septum formation. In the class IIIB (bldA) mutant, DNA segregation appeared to be uncoupled from septum formation. The results indicate that the class III mutants are defective in loci that are involved in the regulation of key events of Streptomyces morphogenesis.Streptomyces sporulation is characterized by the formation of chains of uninucleoidal spores from multinucleoidal, filamentous cells known as hyphae. The morphological changes that occur during the transition from the vegetatively growing hyphae to the chains of spores have been identified from the examination of strains that are undergoing sporulation on an agar surface. Under this condition, the onset of sporulation is marked by the vertical projection of branches from the vegetative mycelium. After elongation, these aerial hyphae undergo coiling and massive septation to form compartments that are destined to become spores (24). The sporulation septa are double layered, resembling the cell division septa of unicellular bacteria. Each compartment contains at least one copy of the chromosome to ensure spore viability. Subsequently the walls thicken and round up to form the ovoid spores in a chain that is confined within a fibrous sheath that ruptures after the spores mature. The formation of a sporulating colony generally requires at least 48 h of vegetative growth prior to erection of the aerial hyphae, and maturation of the spores can take an additional 2 to 4 days (9,13,15,25). Colonies that are undergoing differentiation comprise vegetative hyphae, lysing hyphae, aerial hyphae, immature and mature spores, and germinating spores (20,23).Because of the heterogeneity of differentiating Streptomyces colonies, limited information can be obtained about the nature and timing of events central to Streptomyces sporulation. To overcome this limitation, we have turned to the analysis of sporulation in liquid culture (submerged sporulation) by Streptomyces griseus. With this organism, submerged sporulation can be induced by phosphate or nitrogen starvation (10) or nutritional downshift (transfer to a nutrient-replete, minimal medium [11]) but not by carbon starvation (10). Submerged sporulation is not only rapid but also essentially synchronous. Thus, this technique was likely to...
Abnormalities in G-protein-gated inwardly rectifying potassium (GIRK) channels have been implicated in diseased states of the cardiovascular system; however, the role of GIRK4 (Kir3.4) in cardiac physiology and pathophysiology has yet to be completely understood. Within the heart, the KACh channel, consisting of two GIRK1 and two GIRK4 subunits, plays a major role in modulating the parasympathetic nervous system’s influence on cardiac physiology. Being that GIRK4 is necessary for the functional KACh channel, KCNJ5, which encodes GIRK4, it presents as a therapeutic target for cardiovascular pathology. Human variants in KCNJ5 have been identified in familial hyperaldosteronism type III, long QT syndrome, atrial fibrillation, and sinus node dysfunction. Here, we explore the relevance of KCNJ5 in each of these diseases. Further, we address the limitations and complexities of discerning the role of KCNJ5 in cardiovascular pathophysiology, as identical human variants of KCNJ5 have been identified in several diseases with overlapping pathophysiology.
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