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Biomedical subjects

P Linder

Publications and source records attributed to P Linder.

66 records · Page 4Linked to original sources
PubMed1985

An essential replication gene, repA, of plasmid pSC101 is autoregulated.

Measurements of the rate of replication of a mutant pSC101 plasmid, cloned into a ColE1 vector, showed that insertions of the transposon Tn1000 into the repA gene of pSC101 abolished replication activity, but could be complemented in trans, albeit at a low level. The promoter of the repA gene was mapped by the construction of repA-lacZ gene fusions, and one of the fusions was used to demonstrate that repA protein, provided in trans, could repress expression of beta-galactosidase activity. This repression was primarily due to reduction of transcription of the repA-lacZ fusion. The sequence analysis of mutants of the repA-lacZ fusion gene which were no longer sensitive to the presence of repA protein showed that the site of action of repA was a 22 base-pair sequence, present as an inverted repeat, overlapping the repA promoter. The repA gene is thus autoregulated.

Bacterial Proteins↗
PubMed1984

Replication functions encoded by the plasmid pSC101.

We describe the mapping of several genetic loci involved in the replication of the pSC101 plasmid. These include the origin of replication and a short segment of DNA that encodes a pSC101 incompatibility function. This short segment lies within the origin region. Flanking the incompatibility segment are two loci, repA and repB, which are required for replication. The product of the repA locus is shown to be trans-acting.

Bacterial Proteins↗
PubMed1983

Plasmid pSC101 replication mutants generated by insertion of the transposon Tn1000.

A derivative of pSC101, pLC709, was constructed by ligation of the HincII-A fragment of pSC101 to the mini-colEI plasmid pVH51 and to a DNA fragment encoding resistance to the antibiotics streptomycin and spectinomycin. Insertions of the transposon Tn1000 (gamma-delta) into the pSC101 replication region of pLC709 were isolated following cotransfer of the plasmid with the sex factor F. The sites of insertion of the transposon were determined by restriction enzyme analysis and the replication and incompatibility properties of the insertion plasmids and DNA fragments cloned from them were analysed. The insertion mutations defined a locus, inc, of approximately 200 base-pairs that is responsible for pSC101-specific incompatibility. Two mutations adjacent to this region inactivate pSC101 replication but can be complemented in trans by a wild-type pSC101 plasmid, and thus define a trans-acting replication function, rep. The inc locus is within a larger region of some 450 base-pairs that is essential for pSC101 replication and that includes the origin of replication. This 450 base-pair segment can replicate in the presence of a helper plasmid that supplies the rep function in trans.

DNA Replication↗
PubMed1983

The nucleotide sequence of replication and maintenance functions encoded by plasmid pSC101.

The nucleotide sequence of 1100bp around the origin of replication of the pSC101 plasmid has been determined. This segment of DNA is capable of replication in the presence of a helper plasmid. The sequence data reveal similarities between pSC101 and several other replicons. The origin of replication contains three direct repeats of an 18bp sequence associated with a segment exceptionally rich in A-T base pairs. A promotor that probably directs transcription of a gene encoding an essential plasmid replication function is associated with a region of extensive potential secondary structure. The sequence presented here includes the sequence of the par region involved in partitioning of plasmids at cell division.

Base Composition↗
PubMedDate not supplied

NMR in vitro effects on proliferation, apoptosis, and viability of human chondrocytes and osteoblasts.

This study presents findings on the proliferation rate, cellular apoptosis, and viability of human chondrocyte and osteoblast cultures before and after treatment with NMR pulse sequences. A commercially available nuclear magnetic resonance machine (MBST(R)-Nuclear Magnetic Resonance Therapy) was used for treatment. The study was carried out for 19 days, including 9 days of NMR exposure in a controlled, double-blind, randomized manner, using commercially available human cell lines. The study revealed that NMR treatment did not induce apoptosis or inhibit cell viability, but revealed a tendency of an elevated cell proliferation rate as observed by cell count.

Apoptosis↗