Replication and temperature-sensitive maintenance functions of lactose plasmid pSK11L from Lactococcus lactis subsp. cremoris.

The replication region of pSK11L, the lactose plasmid of Lactococcus lactis subsp. cremoris (L. cremoris) SK11, was isolated on a 14.8-kbp PvuII fragment by shotgun cloning into an Escherichia coli vector encoding erythromycin resistance and selection for erythromycin-resistant transformants of L. lactis subsp. lactis (L. lactis) LM0230. Deletion analysis and Tn5 mutagenesis of the resulting plasmid (pKMP1) further localized the replication region to a 2.3-kbp ScaI-SpeI fragment. DNA sequence analysis of this 2.3-kbp fragment revealed a 1,155-bp open reading frame encoding the putative replication protein, Rep. The replication origin was located upstream of rep and consisted of an 11-bp imperfect direct repeat and a 22-bp sequence tandemly repeated three and one-half times. The overall organization of the pSK11L replicon was remarkably similar to that of pCI305, suggesting that pSK11L does not replicate by the rolling-circle mechanism. Like pSK11L, pKMP1 was unstable in L. lactis LM0230. Deletion analysis allowed identification of several regions which appeared to contribute to the maintenance of pKMP1 in L. lactis LM0230. pKMP1 was significantly more stable in L. cremoris EB5 than in L. lactis LM0230 at all of the temperatures compared. This stability was lost by deletion of a 3.1-kbp PvuII-XbaI fragment which had no effect on stability in L. lactis LM0230. Other regions affecting stability in L. cremoris EB5 but not in L. lactis LM0230 were also identified. Stability assays conducted at various temperatures showed that pKMP1 maintenance was temperature sensitive in both L. lactis LM0230 and L. cremoris EB5, although the plasmid was more unstable in L. lactis LM0230. The region responsible for the temperature sensitivity phenotype in L. lactis LM0230 was tentatively localized to a 1.2-kbp ClaI-HindIII fragment which was distinct from the replication region of pSK11L. Our results suggest that the closely related L. lactis and L. cremoris subspecies behave differently regarding maintenance of plasmids.     

The Epidemiology of Dental Diseases in the Elderly1

This paper summarizes and evaluates epidemiologic evidence on adult dental conditions with a focus on older adults. Information is presented on coronal caries; root caries; loss of teeth, attrition, abrasion, and erosion; periodontal diseases; and oral cancer. The author concludes that the oral health status of the elderly in the United States is essentially unknown. There are no recent, representative population base studies of oral conditions in the elderly. Studies of prevalence or incidence of oral diseases typically include few elderly persons or describe a select group of elderly who are at high risk. Furthermore, it is not really known whether the incidence and prevalence of coronal caries or root caries is actually increasing or is part of a cohort effect. While oral cancers have been shown to increase with age, there is no information as to whether their incidence rates are increasing. While, clinically, there are indications that attrition, abrasion and erosion are characteristics that are more likely to be seen in older adults, there is no information about their distribution in the population. There is evidence that loss of teeth is decreasing but nothing is known about the patterning of that loss. As for periodontal diseases, much work is needed to identify various syndromes that may be distinguished by their distribution in the population as well as determining whether periodontitis is a condition responsible for a majority of tooth loss or just the majority of tooth loss in a small high risk group. In addition, some suggestions are presented for future directions of research in this area.     

THE SUSCEPTIBILITY OF THE PLANT CELL TO VIRUS DISEASE

A number of spraying experiments showed that the virus cannot enter a plant unless some of the cells are injured. It is not essential that such injury should be brought about in the presence of the virus. The chances of infection fall off rapidly in the first few minutes after injury, but infection occurs occasionally as long as half an hour after the cell is damaged.
Inoculations by micropipette into single cells of the host plant yielded only about one-tenth of the expected number of infections. This suggests differences in the susceptibility of the cells to virus attack.