PubMed · 4894473
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J T August, L Shapiro. 1968. Ribonucleic acid virus replication.. https://pubmed.ncbi.nlm.nih.gov/4894473/
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We report here the use of a PCR based assay modified by us for the detection of Salmonella spp. in foods, based on amplification of a 236 bp Salmonella specific hin/H2 region [Way et al. (1993) Applied and Environmental Microbiology 59, 1473-1479], using Ampli Taq Gold polymerase. Using this assay we were able to detect all the Salmonella serovars tested. The limit of detection was 1 fg of purified target DNA or N x 10(0) (1-3 cells) cfu ml(-1) of pure bacterial culture. This assay could detect N x 10(0) cfu Salmonella cells g(-1) of the food sample unambiguously in presence of endogenous microflora following 6 h enrichment, thus requires a duration of approximately 10 h for the full processing from DNA template preparation, PCR and visualization of DNA product on agarose gel. The main advantage of this PCR detection method is its sensitivity, and specificity. We also tried to adopt DNA template isolation method simply by boiling the bacterial cells thereby reducing the possibility of contamination, cutting the processing time and cost considerably. This can be an added advantage for the use of this system in simple lab setups.
Selectable marker genes are required to ensure the efficient genetic modification of crops. Economic incentives and safety concerns have prompted the development of several strategies (site-specific recombination, homologous recombination, transposition, and co-transformation) to eliminate these genes from the genome after they have fulfilled their purpose. Recently, chemically inducible site-specific recombinase systems have emerged as valuable tools for efficiently regulating the excision of transgenes when their expression is no longer required. The implementation of these strategies in crops and their further improvement will help to expedite widespread public acceptance of agricultural biotechnology
Omenn syndrome (OS) is an inherited disorder characterized by an absence of circulating B cells and an infiltration of the skin and the intestine by activated oligoclonal T lymphocytes, indicating that a profound defect in the lymphoid developmental program could be accountable for this condition. Inherited mutations in either the recombination activating genes RAG1 or RAG2, resulting in partial V(D)J recombinase activity, were shown to be responsible for OS. This study reports on the characterization of new RAG1/2 gene mutations in a series of 9 patients with OS. Given the occurrence of the same mutations in patients with T-B-severe combined immune deficiency or OS on 3 separate occasions, the proposal is made that an additional factor may be required in certain circumstances for the development of the Omenn phenotype. The nature of this factor is discussed.