Model for homologous recombination during transfer of DNA into mouse L cells: role for DNA ends in the recombination process.

Lin, F L; Sperle, Karen; Sternberg, Nat

doi:10.1128/mcb.4.6.1020

Cited by 414 publications

(374 citation statements)

References 23 publications

Supporting

Mentioning

351

Contrasting

Unclassified

Order By: Relevance

“…In previous experiments we observed in vivo recombination at a 5 bp homology between enhancer trap and enhancer fragment (Weber et al, 1984). Such homologous recombination events occur more frequently with linear substrate DNAs than with circular DNAs (Lin et al, 1984;P. Pfeiffer, J. de Villiers, and W. Schaffner, unpublished).…”

Section: Nucleotide Sequence Of the Hcmv Enhancer And Localization Rementioning

confidence: 74%

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

Boshart

Weber

Jahn

et al. 1985

Cell

1,098

648

View full text Add to dashboard Cite

SummaryA strong transcription enhancer was identified in the genomic DNA (235 kb) of human cytomegalovirus (HCMV), a ubiquitous and severe pathogen of the herpesvirus group. Cotransfection of enhancerless SV40 DNA with randomly fragmented HCMV DNA yielded two SV40-HCMV recombinant viruses that had incorporated overlapping segments of HCMV DNA to substitute for the missing SV40 enhancer. Within HCMV, these enhancer sequences are located upstream of the transcription initiation site of the major immediate-early gene, between nucleotides -118 and -524. Deletion studies with the HCMV enhancer, which harbors a variety of repeated sequence motifs, show that different subsets of this enhancer can substitute for the SV40 enhancer. The HCMV enhancer, which seems to have little cell type or species preference, is severalfold more active than the SV40 enhancer. It is the strongest enhancer we have analyzed so far, a property that makes it a useful component of eukaryotic expression vectors.

show abstract

Section: Nucleotide Sequence Of the Hcmv Enhancer And Localization Rementioning

confidence: 74%

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

Boshart

Weber

Jahn

et al. 1985

Cell

1,098

648

View full text Add to dashboard Cite

show abstract

“…Errors in this process would lead to the replacement of the excised element by a mutated copy, i.e., a new Ds element. We therefore conclude that, typically, Ds formation occurs through homologous recombination between the broken donor site and its homologous region, and we rule out DSB repair mechanisms that do not involve DNA synthesis, such as the single strand annealing (SSA) model (31) or end-joining of broken ends at the donor site (52,54).…”

Section: Discussionmentioning

confidence: 99%

Abortive Gap Repair: Underlying Mechanism for Ds element Formation

Rubin

Levy

1997

Molecular and Cellular Biology

114

View full text Add to dashboard Cite

The mechanism by which the maize autonomous Ac transposable element gives rise to nonautonomous Ds elements is largely unknown. Sequence analysis of native maize Ds elements indicates a complex chimeric structure formed through deletions of Ac sequences with or without insertions of Ac-unrelated sequence blocks. These blocks are often flanked by short stretches of reshuffled and duplicated Ac sequences. To better understand the mechanism leading to Ds formation, we designed an assay for detecting alterations in Ac using transgenic tobacco plants carrying a single copy of Ac. We found frequent de novo alterations in Ac which were excision rather than sequence dependent, occurring within Ac but not within an almost identical Ds element and not within a stable transposase-producing gene. The de novo DNA rearrangements consisted of internal deletions with breakpoints usually occurring at short repeats and, in some cases, of duplication of Ac sequences or insertion of Ac-unrelated fragments. The ancient maize Ds elements and the young Ds elements in transgenic tobacco showed similar rearrangements, suggesting that Ac-Ds elements evolve rapidly, more so than stable genes, through deletions, duplications, and reshuffling of their own sequences and through capturing of unrelated sequences. The data presented here suggest that abortive Ac-induced gap repair, through the synthesis-dependent strand-annealing pathway, is the underlying mechanism for Ds element formation.Dissociation, or Ds, is the first discovered transposable element (TE). It was identified as a maize locus on chromosome 9, where breaks occur in the presence of Activator (Ac), a second gene found at a separate locus (33,34). Subsequent studies showed that Ac can transpose autonomously whereas Ds moves only in the presence of Ac (35,36). In addition, Ac activity can turn into a Ds type of instability, while no occurrences were found of Ds turning into Ac (37, 38). On the basis of these observations, McClintock proposed that Ds nonautonomous elements are derived from Ac through mutations (39). The proposal that Ac and Ds are phylogenetically related has been supported by molecular analysis, as described below, but the mechanism responsible for the conversion of Ac into Ds is still unknown.Ac is a 4.6-kb-long element flanked by 11-bp terminal inverted repeats (TIRs) (12). It encodes an 807-amino-acid protein, the transposase, necessary for both Ac and Ds transposition (28). Ds elements, on the other hand, do not encode a functional transposase but retain regions which are essential for their transposition (6). There are six fully sequenced Ds elements, all of which share with Ac nearly identical TIRs and fall into the following four categories: (i) those with nearly no similarity to Ac, like Ds1 (57); (ii) elements with highly similar subterminal regions but with internal deletions, like Ds9 (46); (iii) double Ds elements where one internally deleted Ds is inserted into another identical Ds in an inverted orientation (9); and (iv) Ds elements that contain bot...

show abstract

“…Thus, when the replication fork hits a DNA lesion or a nick at a site undergoing excision or mismatch repair in the template strand, hRad51-mediated strand transfer might be biased towards the newly synthesized 3'-end to initiate recombinational repair utilizing the double-stranded sister DNA as the donor (Cox, 1997;Haber, 1999). In yeast cells, 3' single-stranded ends prevail after processing of DSBs, and represent substrates for the single-stranded annealing (SSA) mechanism or invade a homologous donor sequence during gene conversion (Lin et al, 1984(Lin et al, , 1990White and Haber, 1990;Sun et al, 1991;Sugawara and Haber, 1992). During these two major break repair pathways in S. cerevisiae 3'-ends of DSBs serve as primers for gap-®lling DNA-synthesis.…”

Section: Nucleolytic Processing Of Recombination Intermediates By P53mentioning

confidence: 99%

Role of heteroduplex joints in the functional interactions between human Rad51 and wild-type p53

et al. 2000

View full text Add to dashboard Cite

Model for homologous recombination during transfer of DNA into mouse L cells: role for DNA ends in the recombination process.

Cited by 414 publications

References 23 publications

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

Abortive Gap Repair: Underlying Mechanism for Ds element Formation

Role of heteroduplex joints in the functional interactions between human Rad51 and wild-type p53

Contact Info

Product

Resources

About