Open AccessSite-specific inversion sequence of the herpes simplex virus genome: Domain and structural features
Author(s) -
Edward S. Mocarski,
Bernard Roizman
Publication year - 1981
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.78.11.7047
Subject(s) - tandem repeat , direct repeat , genetics , sequence (biology) , biology , inverted repeat , genome , nucleic acid sequence , repeated sequence , dna , consensus sequence , base pair , dna sequencing , gene , base sequence
The genome of herpes simplex virus-1 consists of two covalently linked components, L and S, that invert relative to each other. The L and S components consist of unique DNA sequences bracketed by inverted repeats. The inverted repeats of the L component are designatedab andb ′a ′ and those of the S component are designateda ′c ′ andca . The number ofa sequences at the termini and at the L-S component junction varies from one to several copies. Insertion into the middle of the L component of a DNA fragment consisting of 156 base pairs (bp) of theb sequence, an entirea sequence of 501 bp, and 618 bp of thec sequence created a new site through which additional inversions in the genome occurred. Comparison of the nucleotide sequences of DNA fragments containing one and twoa sequences defined the domain of thea sequence. The singlea sequence consists of two 20-bp direct repeats (designated as DR1) bracketing a region that contains 19 tandem direct repeats of a 12-bp sequence (DR2) adjacent to three direct repeats of a 37-bp sequence (DR4), in addition to short stretches of unique sequences. The fragment with two tandema sequences contained three copies of DR1—i.e., the intervening DR1 was shared by the twoa sequences. Furthermore, onea sequence contained 22 copies of DR2 and two copies of DR4 whereas the seconda sequence contained 19 copies of DR2 and two copies of DR4. These observations suggest that (i ) amplification of the number of terminal and internala sequences is the consequence of intramolecular or intermolecular recombination through DR1, (ii ) the number of copies of DR2 and DR4 within thea sequence is not fixed and may vary as a consequence of unequal crossing over or slippage, and (iii ) inversion results from intramolecular recombination between terminal and inverteda sequences.