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The sarcoplasmic reticulum (SR) of striated muscle plays a central role in control of contractile activity. It acts as an intracellular sink for calcium during relaxation and releases cav2 + during contraction. This highly differentiated endoplasmic reticulum is a self-contained network with a continuous hollow interior which surrounds each muscle fibril (Fig. 1) (Porter, 1961). The SR is fragmented at longitudinal intervals of one sarcomere in length by the transverse tubular or T-tubular system (Porter, 1961; Franzini-Armstrong, 1980). On each side of the T-tubules there are enlarged areas known as cisternae, with branched areas between the cisternae known as the longitudinal elements. The juncture of the three membranes (two terminal cisternae and one Ttubule) is referred to as the triad. The junction between the SR and • 0 the T-tubules is known as a junctional gap and has.a width of 100-200 A. Periodic densities, referred to as 'feet', cross the junctional gap to join the SR and T-tubular membranes (Franzini-Armstrong, 1980). Direct communication between the SR, the T-tubules and the feet have been postulated (Schneider· and Chandler, 1973; Mathias et al., 1979). The view has developed, starting with the experiments of Huxley and Taylor (1958) and Huxley and Straub (1958), that, under physiological conditions, contraction in skeletal muscle is triggered by depolarisation of the membranes of the T-tubules. This results in the release of ca 2 + into the myoplasm from its intracellular storage location, the SR, and thus activating the contractile proteins (Schneider and Chandler, 1973). (See Fuchs (1974) and Ebashi (1980) for a review on the possible mechanism involved in excitation-contraction coupling.)

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Thesis (Ph. D.)--University of Wisconsin--Madison, 1969. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliography.

Nuclear bone morphogenetic protein 2 (nBMP2) is a nuclear variant of the secreted growth factor BMP2. Experiments in nBmp2NLStm mutant mice, which lack nBMP2 in the nucleus, have shown that nBMP2 affects intracellular calcium transport in skeletal muscle and hippocampal neurons. The objective of this study was to determine whether nBMP2 affects the immune system, since activation of lymphocytes and other immune cells depends on intracellular calcium transport. We found that spleens in nBmp2NLStm mutant mice were 24% smaller than in wild type mice. The white pulp of the spleen contains many immune cells, particularly B and T lymphocytes and reduced spleen size in the nBmp2NLStm mutant mice could be caused by a reduced number of lymphocytes migrating to the spleen. When mutants and wild types were challenged with an intravenous infection of 10^7 CFU of S. aureus, they showed similar immune responses. Samples of blood, liver, spleen, kidney and lymph nodes cultured three days after infection showed no difference in post infection bacterial load between mutant and wild type. Likewise, post-infection weight loss and percent survival were similar between mutant and wild type, suggesting that the innate immune response is functional in nBmp2NLStm mice. However, when mice were challenged with a secondary infection, immune response and spleen function were severely impaired. Mutant mice showed higher levels of bacteria remaining in the blood and had lower rate of survival to day 3 after secondary infection. In addition, CD4+ and CD8+ T-cell levels within mutant lymph nodes were significantly reduced, indicating that nBMP2 is involved in the secondary immune response.

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