We have isolated 40 mutants of Escherichia coli which are nonchemotactic as judged by their failure to swarm on semisolid tryptone plates or to make bands in capillary tubes containing tryptone broth. All the mutants have normal flagella, a fact shown by their shape and reaction with antiflagella serum. All are fully motile under the microscope and all are sensitive to the phage chi. Unlike its parent, one of the mutants, studied in greater detail, failed to show chemotaxis toward oxygen, glucose, serine, threonine, or aspartic acid. The failure to exhibit chemotaxis does not result from a failure to use the chemicals. The swimming of this mutant was shown to be random. The growth rate was normal under several conditions, and the growth requirements were unchanged.
We have re-examined some of the factors affecting the induction of heart-forming mesoderm in the axolotl. The formation of functional, rhythmically contracting myocardial tissue was used as an assay. We have found that heart-forming mesoderm is fully induced and capable of completing its developmental repertoire by the end of neurulation. As has been previously reported, pharyngeal endoderm appears to be the major inductor of heart mesoderm. Unlike previous workers, we have found that the inducing activity appears to be highly localized in the mid-ventral pharyngeal endoderm. The endoderm retains its inductive properties, and the mesoderm retains at least some capacity to respond, long after the heart-forming mesoderm is apparently fully induced. We have also found that RNA extracts from pharyngeal endoderm, which are capable of causing cardiac-lethal (c/c) mutant axolotl hearts to begin beating, are not capable of inducing early wild-type heart-forming mesoderm. Based on these results, we speculate that induction of heart-forming mesoderm is a two-step process. The first signal, occurring during neurulation, directs the mesoderm to begin differentiating into cardiomyocytes, and the second, beginning in mid- to late neurulation and continuing until just prior to the onset of heartbeat, causes myofibrillogenesis and the initiation of rhythmic contractions. The latter signal, which is lacking in c/c mutant embryos, appears to be necessary to override an inhibition present in the embryonic milieu.
During exponential growth, strain AW405 of Escherichia coli K-12 did not regulate the fatty acid composition of its lipids in response either to temperature or to the addition of NaCl, KCl, or MgCl2 to the medium. Growth was severely restricted at temperatures below 21 degrees C. Differential scanning calorimetry (DSC) of the isolated lipids from a culture with a typical exponential-phase composition yielded a broad transition, extending from approximately 0 to 33 degrees C, with a midpoint at 19 degrees C. During late stages of growth, the fatty acid composition changed. The percentage of palmitic acid increased and cyclopropane fatty acids replaced some of the equivalent unsaturated fatty acids. The increase in palmitate seemed largely independent of growth conditions, whereas the increase in the cyclopropane fatty acids was stimulated by the addition of salts or sucrose. Cultures grown in the presence of sucrose also had higher cyclopropane fatty acid levels during exponential growth. DSC of lipids from a sucrose culture, in which the compositional changes were most pronounced, yielded a much narrower transition with a midpoint at 27 degrees C.
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