In the first four years of the LHD experiment, several encouraging results have emerged, the most significant of which is that MHD stability and good transport are compatible in the inward shifted axis configuration. The observed energy confinement at this optimal configuration is consistent with ISS95 scaling with an enhancement factor of 1.5. The confinement enhancement over the smaller heliotron devices is attributed to the high edge temperature. We find that the plasma with an average beta of 3% is stable in this configuration, even though the theoretical stability conditions of Mercier modes and pressure driven low-n modes are violated. In the low density discharges heated by NBI and ECR, internal transport barrier (ITB) and an associated high central temperature (>10 keV) are seen. The radial electric field measured in these discharges is positive (electron root) and expected to play a key role in the formation of the ITB. The positive electric field is also found to suppress the ion thermal diffusivity as predicted by neoclassical transport theory. The width of the externally imposed island is found to decrease when the plasma is collisionless with finite beta and increase when the plasma is collisional. The ICRF heating in LHD is successful and a high energy tail (up to 500 keV) has been detected for minority ion heating, demonstrating good confinement of the high energy particles. The magnetic field line structure unique to the heliotron edge configuration is confirmed by measuring the plasma density and temperature profiles on the divertor plate. A long pulse (2 min) discharge with an ICRF power of 0.4 MW has been demonstrated and the energy confinement characteristics are almost the same as those in short pulse discharges.

Incomplete flagellar structures were detected in osmotically shocked cells or membrane-associated fraction of many nonflagellate mutants of Salmonella typhimurium by electron microscopy. The predominant types of these structures in the mutants were cistron specific. The incomplete basal bodies were detected in flaFI, flaFIV, flaFVIII, and flaFIX mutants, the structure homologous to a basal body in flaFV mutants, the polyhook-basal body complex in flaR mutants, and the hook-basal body complex in flaL and flaU mutants. No structures homologous to flagellar bases or their parts were detected in the early-fla group nonflagellate mutants of flaAI, flaAII, flaAIII, flaB, flaC, flaD, flaE, flaFII, flaFIII, flaFVI, flaFVII, flaFX, flaK, and flaM. From these observations, a process of flagellar morphogenesis was postulated. The functions of the early-fla group are essential to the formation of S ring-M ring-rod complexes bound to the membrane. The completion of basal bodies requires succeeding functions of flaFI, flaFIV, flaFVIII, and flaFIX. Next, the formation of hooks attached to basal bodies proceeds by the function of flaFV and by flaR, which controls the hook length. Flagellar filaments appear at the tips of hooks because of the functions of flaL, flaU, and flagellin genes.

Escherichia coli mutants with defects in 29 flagellar genes identified so far were examined by electron microscopy for possession of incomplete flagellar structures in membrane-associated fractions. The results are discussed in consideration of the known transcriptional interaction of flagellar genes. Hook-basal body structures were detected in flaD, flaS, flaT, flbC, and hag mutants. The flaE mutant had a polyhook-basal body structure. An intact basal body appeared in flaK mutants. Putative precursors of the basal body were detected in mutants with defects in flaM, flaU, flaV, and flaY. No structures homologous to the flagellar basal body or its parts were detected in mutants with defects in flaA, flaB, flaC, flaG, flaH, flaI, flaL, flaN, flaO, flaP, flaQ, flaR, flaW, flaX, flbA, flbB, and flbD. One flaZ mutant had an incomplete flagellar basal body structure and another formed no significant structure, suggesting that flaZ is responsible for both basal body assembly and the transcription of the hag gene.

Global transcriptional responses to dehydration and rehydration were determined in Anabaena sp. PCC 7120. Nearly 300 genes were up-or downregulated during both dehydration and rehydration. While as many as 133 genes showed dehydration-specific downregulation, only 29 genes showed dehydration-specific upregulation. In contrast, while only 13 genes showed rehydration-specific downregulation, as many as 259 genes showed rehydration-specific upregulation. The genes upregulated during rehydration responded rapidly and transiently, whereas those upregulated during dehydration did so gradually and persistently. The expression of various genes involved in DNA repair, protein folding and NAD synthesis, as well as genes responding to nitrogen depletion and CO 2 limitation, was upregulated during rehydration. Although no genes for transcriptional regulators showed dehydration-specific upregulation, eight showed rehydration-specific upregulation. Among them, two genes, ancrpB and alr0618, encode putative transcriptional activators of the cAMP receptor protein (CRP) family. DNA microarray analysis using gene disruptants revealed that AnCrpB and Alr0618 regulate the genes induced by nitrogen depletion and by CO 2 limitation, respectively. We conclude that rehydration is a complex process in which the expression of certain genes, particularly those for metabolism, is dramatically induced.