Christian Lavialle, CNRS UMR8122, Institut Gustave Roussy, 94805 Villejuif, France
30 March 2012
Upon reading each of the commentaries published in Retrovirology (9:23, 9:24 and 9:25) on March 22, 2012, about the debated identity of the Emv2 endogenous retrovirus of C57BL6 mice, it appeared to me that none of the authors seemed to be aware of previously published data that I believe contain all the information required to settle the matter.
Indeed, in a paper published in 2006 (Int. J. Cancer 119, 1869-1877), Potlichet, Mangeney and Heidmann had already precisely identified the Emv-2 provirus within the genome of C57BL6 mice by both Southern blotting with an ecotropic MLV-specific probe and nucleotide sequence comparisons. They reported that the melanoma-associated retrovirus (MelARV) expressed in the B16 mouse melanoma is a recombinant between the Emv-2 endogenous retrovirus present in the genome of C57BL6 mice at the position of chromosomal band 8qE1 and a provirus located in the qA3 region of chromosome 5. The authors stated that sequence alignments of MelARV with the endogenous Emv-2 and a chromosome 5 provirus provided evidence that the Emv-2 provirus was the prime contributor to the backbone of MelARV, sharing with it more than 99.8% nucleotide sequence identity, except for two small gag (367 nt) and pol (416 nt) regions that were provided by the chromosome 5 endogenous provirus (see Figure 3 in the reference mentioned above). Using the MelARV sequence (accession number U63133 or DQ366149) as a BLAST query on the mouse genome (NCBI build 37.1), a unique highly homologous region consistent with Emv-2 is found at exactly the same position as that given for the so-called ERVmch8. All the other matching loci have only 90% or less nucleotide similarity. Thus, ERVmch8 and Emv-2 are unambiguously one and the same.
Competing interests
The author declares that he has no competing interests.
Emv2
Christine Kozak, NIH
5 April 2012
It is clear that the C57BL Emv described in the paper you referenced (Int. J. Cancer 2006 119:1869-1877) is Emv2. The HindIII fragment size in Fig 2 is comparable to that described for Emv2 by Jenkins and colleagues (J Virology 1982, 43:26-36), and, as pointed out earlier (Retrovirology 9:23 and 9:25), BLAST searches with either E-MLV env specific sequences or the full length E-MLV genome identify a single nearly identical sequence in C57BL on distal Chromosome 8, as is also the case with the search you described using the recombinant MelARV. The paper by Lee and colleagues (Retrovirology 8:82, 2011) also noted the high degree of sequence identity between Emv2 and the Emv2-derived MelARV.
My comment emphasized only two factors ¿ Emv2 expression and map location. With regard to the latter, I note that the MelARV paper provided a cytogenetic map location for Emv2 (8qE1), along with more specific information on its chromosomal position relative to a newly acquired insertion, and this position is consistent with the Emv2 map location based on the earlier linkage analyses.
Competing interests
The author declares that she has no competing interests.
Emv2 and ERVmch8 are one and the same
30 March 2012
Upon reading each of the commentaries published in Retrovirology (9:23, 9:24 and 9:25) on March 22, 2012, about the debated identity of the Emv2 endogenous retrovirus of C57BL6 mice, it appeared to me that none of the authors seemed to be aware of previously published data that I believe contain all the information required to settle the matter.
Indeed, in a paper published in 2006 (Int. J. Cancer 119, 1869-1877), Potlichet, Mangeney and Heidmann had already precisely identified the Emv-2 provirus within the genome of C57BL6 mice by both Southern blotting with an ecotropic MLV-specific probe and nucleotide sequence comparisons. They reported that the melanoma-associated retrovirus (MelARV) expressed in the B16 mouse melanoma is a recombinant between the Emv-2 endogenous retrovirus present in the genome of C57BL6 mice at the position of chromosomal band 8qE1 and a provirus located in the qA3 region of chromosome 5. The authors stated that sequence alignments of MelARV with the endogenous Emv-2 and a chromosome 5 provirus provided evidence that the Emv-2 provirus was the prime contributor to the backbone of MelARV, sharing with it more than 99.8% nucleotide sequence identity, except for two small gag (367 nt) and pol (416 nt) regions that were provided by the chromosome 5 endogenous provirus (see Figure 3 in the reference mentioned above). Using the MelARV sequence (accession number U63133 or DQ366149) as a BLAST query on the mouse genome (NCBI build 37.1), a unique highly homologous region consistent with Emv-2 is found at exactly the same position as that given for the so-called ERVmch8. All the other matching loci have only 90% or less nucleotide similarity. Thus, ERVmch8 and Emv-2 are unambiguously one and the same.
Competing interests
The author declares that he has no competing interests.
Emv2
5 April 2012
It is clear that the C57BL Emv described in the paper you referenced (Int. J. Cancer 2006 119:1869-1877) is Emv2. The HindIII fragment size in Fig 2 is comparable to that described for Emv2 by Jenkins and colleagues (J Virology 1982, 43:26-36), and, as pointed out earlier (Retrovirology 9:23 and 9:25), BLAST searches with either E-MLV env specific sequences or the full length E-MLV genome identify a single nearly identical sequence in C57BL on distal Chromosome 8, as is also the case with the search you described using the recombinant MelARV. The paper by Lee and colleagues (Retrovirology 8:82, 2011) also noted the high degree of sequence identity between Emv2 and the Emv2-derived MelARV.
My comment emphasized only two factors ¿ Emv2 expression and map location. With regard to the latter, I note that the MelARV paper provided a cytogenetic map location for Emv2 (8qE1), along with more specific information on its chromosomal position relative to a newly acquired insertion, and this position is consistent with the Emv2 map location based on the earlier linkage analyses.
Competing interests
The author declares that she has no competing interests.