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J Zenthon

Publications and source records attributed to J Zenthon.

8 recordsLinked to original sources

Extent of the mouse t complex and its inversions shown by in situ hybridization.

Probes for loci situated near one end of the proximal (Tcp-1) and distal (Qa-2, 3) inversions of the mouse t complex have been hybridized to chromosomes of mice with and without t complexes and with morphologically distinguishable chromosome 17s. Both the probe for Tcp-1 and that for Qa-2, 3 hybridized to clearly different positions on t and non-t chromosomes, thus making visible the extent of the two inversions. The proximal inversion extends from roughly the junction of bands A1 and A2 to band A3, and the distal inversion from band A3 to band C. Thus, the whole t complex extends from the band A1-A2 junction to band C, and is therefore somewhat larger than previously thought, and occupies about 1.2% of the genome. A probe for complement component 3 (C3-1), genetically known to be several cM distal to the t complex, was found by in situ hybridization to lie in band E1. The proximal part of chromosome 17 is one of the best known parts of the mouse genome, at both the genetic and molecular levels. It may soon be possible to correlate the length of the t complex in terms of chromosomal distance with its physical length in megabases.

Animals

Localization of the Hprt locus by in situ hybridization and distribution of loci on the mouse X-chromosome.

The hypoxanthine phosphoribosyltransferase locus (Hprt) of the mouse has been localized by in situ hybridization to band XA6. Comparison of the distributions of known loci on the genetic and cytogenetic maps of the X-chromosome suggests some chiasma localization with a relatively high frequency of chiasmata in the F bands. In the A bands there appear to be fewer known loci than expected, but no evidence has been found so far of excessive chiasma formation.

Animals

Lack of inactivation of a mouse X-linked gene physically separated from the inactivation centre.

Previous evidence had shown that, when a mammalian X-chromosome is broken by a translocation, only one of the two X-chromosome segments shows cytological signs of X-inactivation in the form of late replication or Kanda staining. In the two mouse X-autosome translocations T(X;4)37H and T(X;11)38H the X-chromosome break is in the A1-A2 bands; in both, the shorter translocation product fails to exhibit Kanda staining. By in situ hybridization, the locus of ornithine carbamoyltransferase (OCT) was shown to be proximal to the breakpoint (i.e. on the short product) in T37H and distal to the breakpoint in T38H. Histochemical staining for OCT showed that in T38H the locus of OCT undergoes random inactivation, as in a chromosomally normal animal, whereas in T37H the OCT locus remains active in all cells. The interpretation is that, when a segment of X-chromosome is physically separated from the X-inactivation centre, it fails to undergo inactivation. This point is important for the understanding of the mechanism of X-inactivation, since it implies that inactivation is a positive process, brought about by some event that travels along the chromosome. It is also relevant to the interpretation of the harmful effects of X-autosome translocations and the abnormalities seen in individuals carrying such translocations.

Animals

Delayed-type hypersensitivity reaction to H-Y antigen in mice. Effects of soluble antigen from Sertoli cells.

The delayed-type hypersensitivity (DTH) response to the H-Y antigen was investigated in female mice which had been pre-treated with soluble or insoluble H-Y antigen. The present results suggest that Sertoli cells, cultured in vitro, release a factor which, if highly soluble, induces tolerance to male spleen cells. Mice showing marked DTH produced high titre H-Y antibodies after further injections of spleen cells from syngeneic males.

Animals