An Escherichia coli K12 mutant resistant to thymineless death (TLD) was isolated, and its genetic analysis led us to identify a new mutation (recQ1) located between corA and metE on the standard linkage map. The mutation was found to result in increased sensitivity to ultraviolet light and deficiency in conjugational recombination when placed in the recBC sbcB background, indicating that it blocked the RecF pathway of recombination. It seemed likely that this mutation is also capable of causing partial resistance to TLD, but we reserve the possibility of a separate mutation closely linked to recQ1 giving rise to this phenotype. The original mutant was shown to carry an additional mutation probably in the vicinity of the uhp locus, which was also required for the full TLD resistance of the mutant to be expressed.

In an approach to characterizing the nature of the lethal event in thymineless death (TLD), rec mutants of Escherichia coli K12 were examined for their sensitivity to TLD. The recB21 and recC22 mutations sensitized cells of the AB1157 line to TLD but not cells of the HF4733 line. This increased sensitivity was not suppressed substantially by either sbcB15 or xonA1 mutation. In contrast, a recF mutation appeared to make cells more resistant to TLD than rec+ cells. Three different recA alleles were shown not to affect TLD appreciably. These results not only provide further support for the view that the site of the lethal event in TLD is cellular DNA, but also strongly suggest the involvement of the recBC and recF gene products in TLD. The apparent indifference of recA mutation implies that the conventional recombination and repair pathways per se are not involved in TLD and that the hypothetical lethal damage to DNA may be unique in nature.

Pellagra is a photosensitivity syndrome characterized by three “D's”: diarrhea, dermatitis, and dementia as a result of niacin deficiency. However, the molecular mechanisms of photosensitivity dermatitis, the hallmark abnormality of this syndrome, remain unclear. We prepared niacin deficient mice in order to develop a murine model of pellagra. Niacin deficiency induced photosensitivity and severe diarrhea with weight loss. In addition, niacin deficient mice exhibited elevated expressions of COX-2 and PGE syntheses (Ptges) mRNA. Consistently, photosensitivity was alleviated by a COX inhibitor, deficiency of Ptges, or blockade of EP4 receptor signaling. Moreover, enhanced PGE2 production in niacin deficiency was mediated via ROS production in keratinocytes. In line with the above murine findings, human skin lesions of pellagra patients confirmed the enhanced expression of Ptges. Niacin deficiency-induced photosensitivity was mediated through EP4 signaling in response to increased PGE2 production via induction of ROS formation.

The zymogram patterns of esterases and catalases of mycobacterial strains were studied using the thin layer agar electrophoresis.Though there were some variations, Mycobacterium hominis, Al. bovis, Al. kansasii, Al. fortuitum, Al. runyonii, Al. avium, M.piaci and M. smegmatis seemed to show species-specific patterns consisting of 2 to 6 esterase bands and one or more catalase bands. The patterns of scotochromogens and nonchromogens were rather variable.

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