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Anti-transfer RNA antibodies in two patients with pulmonary fibrosis, Raynaud's phenomenon and polyarthritis.

Patient W.S. (a 61-year-old woman) and patient T.M. (a 41-year-old man) developed recurrent fevers, polyarthritis, Raynaud's phenomenon and interstitial pulmonary fibrosis without apparent polymyositis. From HeLa cell extracts, sera from both patients immunoprecipitated all species of intact and deproteinised tRNAs. To identify the antibody binding site more precisely, tRNAs transcribed in vitro from cloned Escherichia coli tRNA genes and various mutants were prepared and used as antigens for immunoprecipitation. When the TpsiC loop, or the D loop were deleted, such mutants were not bound by both sera, suggesting that the D and TpsiC loops were required for antibody binding. Abrogation of tRNA binding occurred when 18G of tRNATrp was replaced with 18A to break the tertiary L-shape structure of tRNA. These results strongly suggest that sera from W.S. and T.M. recognise the tertiary conformation of L-shaped tRNA which is constructed with both D and TpsiC loops. These autoantibodies may also serve as a marker for a new subset of patients with connective tissue diseases that is distinct from anti-aminoacyl-tRNA synthetase syndrome.

Arthritis↗

The evolutionary change of the genetic code as restricted by the anticodon and identity of transfer RNA.

The discovery of non-universal genetic codes in several mitochondria and nuclear systems during the part ten years has necessitated a reconsideration of the concept that the genetic code is universal and frozen, as was once believed. Here, the flexibility of the relationship between codons and amino acids is discussed on the basis of the distribution of non-universal genetic codes in various organisms insofar as has been observed to date. Judging from the result of recent investigations into tRNA identity, it would appear that the non-participation of the anticodon in recognition by aminoacyl-tRNA synthetase has significantly influenced the variability of codons.

Animals↗

Altered or increased transfer-RNA methylation in the course of Interferon action on cells in culture?

The induction of the antiviral state by Interferon might reflect the decrease of the rate of biosynthesis, the degradation or the alteration of one or several tRNAs. This could result in rate-limiting concentrations for codons common in viral RNA but rare in host mRNA. Altered methylation of tRNA could be the basis of such a phenomenon. However, we could not find an altered extent of methylation of total tRNA or an altered pattern of methylation, if mixed tRNAs were chromatographed on MAK- or BD-cellulose columns, despite a large range of conditions of pretreatment of chick embryo fibroblast cultures with interferon.

Animals↗