A Two-Unnatural-Base-Pair System toward the Expansion of the Genetic Code

2004 ◽  
Vol 126 (41) ◽  
pp. 13298-13305 ◽  
Author(s):  
Ichiro Hirao ◽  
Yoko Harada ◽  
Michiko Kimoto ◽  
Tsuneo Mitsui ◽  
Tsuyoshi Fujiwara ◽  
...  
Keyword(s):  
Genetic Code ◽  
Base Pair

scholarly journals C-skeleton in the genetic code from a basic series 5 → 0, guiding valences and other numeral features in the code

2021 ◽  
Vol 9 (12) ◽  
Author(s):  
Åsa Wohlin
Keyword(s):  
Amino Acids ◽  
Genetic Code ◽  
Base Pair ◽  
Mean Value ◽  
Atomic Mass ◽  
Side Chain ◽  
Mass Analysis ◽  
Guiding Principle ◽  
Basic Series

The search for regularities in the background for the genetic code and its codon assignments is here further developed, earlier shown to have many correlations with numeral series of integers 5 →0 with different exponents. The atomic mass analysis here counts on 20 + 4 double-coded amino acids, here including Ile AUA as such. A central finding here is that the C-skeleton seems to build on an hierarchical development of the mentioned basic series giving top numbers equal to those returning in side-chain divisions and on first three levels those of C-atoms in base-pair domains. It can very elementary explain the 3/2-division in the weight series. A few main results from earlier articles are shortly recapitulated, since it’s shown here that an x­3-series times 15 (x = integers 5 → 0) joins those earlier aspects and add new ones. It’s found also that atoms with valences 4 + 3 relative those with 2 + 1 make up a 3 to 1-division in both base-pair groups of codon domains, strengthening the earlier observation of valences as one important guiding principle in the relation between codons and domains of amino acids; valences of the atoms which in themselves make up a basic series 5 → 0 in the code when phosphorus P is included. Finally, fundamental factors in the code are gathered, where step 4 →3 seems reign at bottom of the code and number 7, exactly mean value of all atoms.

On the enzymatic incorporation of an imidazole nucleotide into DNA

2017 ◽  
Vol 15 (20) ◽  
pp. 4449-4455 ◽  
Author(s):  
Pascal Röthlisberger ◽  
Fabienne Levi-Acobas ◽  
Ivo Sarac ◽  
Philippe Marlière ◽  
Piet Herdewijn ◽  
...  
Keyword(s):  
Genetic Code ◽  
Base Pair ◽  
Nucleoside Triphosphate ◽  
Metal Base ◽  
Modified Nucleoside

We have evaluated the possibility for using an imidazole modified nucleoside triphosphate for the enzymatic construction of artificial metal base pair with view on an expansion of the genetic code.

scholarly journals Degeneracy of the genetic code and stability of the base pair at the second position of the anticodon

RNA ◽  
2008 ◽  
Vol 14 (7) ◽  
pp. 1264-1269 ◽  
Author(s):  
J. Lehmann ◽  
A. Libchaber
Keyword(s):  
Genetic Code ◽  
Base Pair

scholarly journals Genetic code degeneracy is established by the decoding center of the ribosome

2021 ◽  
Author(s):  
Jean Lehmann ◽  
Shixin Ye
Keyword(s):  
Genetic Code ◽  
Base Pair ◽  
Significant Contribution ◽  
Kinetic Scheme ◽  
Evolutionary Models ◽  
Peptidyl Transferase ◽  
Early Appearance ◽  
Evolutionary Step ◽  
The Stability ◽  
Selection Of

The degeneracy of the genetic code confers a wide array of properties to coding sequences. Yet, its origin is still unclear. A structural analysis has shown that the stability of the Watson-Crick base pair at the second position of the anticodon-codon interaction is a critical parameter controlling the extent of non-specific pairings accepted at the third position by the ribosome, a flexibility at the root of degeneracy. Based on recent cryo-EM analyses, the present work shows that residue A1493 of the decoding center provides a significant contribution to the stability of this base pair, revealing that the ribosome is directly involved in the establishment of degeneracy. Building on existing evolutionary models, we show the evidence that the early appearance of A1493 and A1492 established the basis of degeneracy when an elementary kinetic scheme of translation was prevailing. Logical considerations on the expansion of this kinetic scheme indicate that the acquisition of the peptidyl transferase center was the next major evolutionary step, while the induced-fit mechanism, that enables a sharp selection of the tRNAs, necessarily arose later when G530 was acquired by the decoding center.

Detection of the Glanzmann's Thrombasthenia Mutations in Arab and Iraqi-Jewish Patients by Polymerase Chain Reaction and Restriction Analysis of Blood or Urine Samples

1991 ◽  
Vol 66 (04) ◽  
pp. 500-504 ◽  
Author(s):  
H Peretz ◽  
U Seligsohn ◽  
E Zwang ◽  
B S Coller ◽  
P J Newman
Keyword(s):  
Polymerase Chain Reaction ◽  
Base Pair ◽  
Restriction Analysis ◽  
Urine Samples ◽  
Chain Reaction ◽  
Base Pairs ◽  
Glanzmann’S Thrombasthenia ◽  
Glanzmann's Thrombasthenia ◽  
Base Pair Deletion ◽  
Polymerase Chain

SummarySevere Glanzmann's thrombasthenia is relatively frequent in Iraqi-Jews and Arabs residing in Israel. We have recently described the mutations responsible for the disease in Iraqi-Jews – an 11 base pair deletion in exon 12 of the glycoprotein IIIa gene, and in Arabs – a 13 base pair deletion at the AG acceptor splice site of exon 4 on the glycoprotein IIb gene. In this communication we show that the Iraqi-Jewish mutation can be identified directly by polymerase chain reaction and gel electrophoresis. With specially designed oligonucleotide primers encompassing the mutation site, an 80 base pair segment amplified in healthy controls was clearly distinguished from the 69 base pair segment produced in patients. Patients from 11 unrelated Iraqi-Jewish families had the same mutation. The Arab mutation was identified by first amplifying a DNA segment consisting of 312 base pairs in controls and of 299 base pairs in patients, and then digestion by a restriction enzyme Stu-1, which recognizes a site that is absent in the mutant gene. In controls the 312 bp segment was digested into 235 and 77 bp fragments, while in patients there was no change in the size of the amplified 299 bp segment. The mutation was found in patients from 3 out of 5 unrelated Arab families. Both Iraqi-Jewish and Arab mutations were detectable in DNA extracted from blood and urine samples. The described simple methods of identifying the mutations should be useful for detection of the numerous potential carriers among the affected kindreds and for prenatal diagnosis using DNA extracted from chorionic villi samples.

Mutation Spectrum in Patients with Wiskott-Aldrich Syndrome and X-linked Thrombocytopenia: Identification of Twelve Different Mutations in the WASP Gene

1996 ◽  
Vol 75 (04) ◽  
pp. 546-550 ◽  
Author(s):  
Marianne Schwartz ◽  
Albert Békássy ◽  
Mikael Donnér ◽  
Thomas Hertel ◽  
Stefan Hreidarson ◽  
...  
Keyword(s):  
Base Pair ◽  
Hot Spot ◽  
Missense Mutations ◽  
Nucleotide Substitutions ◽  
Exon 2 ◽  
Wiskott Aldrich Syndrome ◽  
Base Pair Deletion ◽  
Reliable Diagnosis ◽  
Wasp Gene ◽  
Detection Of Mutations

SummaryTwelve different mutations in the WASP gene were found in twelve unrelated families with Wiskott-Aldrich syndrome (WAS) or X-linked thrombocytopenia (XLT). Four frameshift, one splice, one nonsense mutation, and one 18-base-pair deletion were detected in seven patients with WAS. Only missense mutations were found in five patients diagnosed as having XLT. One of the nucleotide substitutions in exon 2 (codon 86) results in an Arg to Cys replacement. Two other nucleotide substitutions in this codon, R86L and R86H, have been reported previously, both giving rise to typical WAS symptoms, indicating a mutational hot spot in this codon. The finding of mutations in the WASP gene in both WAS and XLT gives further evidence of these syndromes being allelic. The relatively small size of the WASP gene facilitates the detection of mutations and a reliable diagnosis of both carriers and affected fetuses in families with WAS or XLT.

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