Misreading Dr. Venter's Genome

Abstract

According to the recent news of the week article “Venter's genome sheds new light on human variation” by J. Cohen (7 September, p. 1311), the annotation of J. Craig Venter's published genome sequence reveals that Dr. Venter is at increased risk for “antisocial behavior.” The gene variant the article is apparently referencing is that of the gene for monoamine oxidase A ( MAOA ) ([1][1]). The table of variants lists Venter's MAOA gene as containing four copies of the uVNTR repeat. Caspi et al. ([2][2]) originally reported that children who were subjected to severe child abuse and who carried the four-uVNTR repeat allele of MAOA were less likely to exhibit antisocial behavior than those with three repeats. If these findings are correct, then Venter is at lower risk, not increased risk, for “antisocial behavior.” The confusion is understandable. Attempts to replicate the original Caspi study have yielded mixed results. Despite contradictory findings, these results have been consistent in several studies: (i) Childhood maltreatment is the strongest predictor of antisocial behavior among the subjects of these studies, and (ii) variation in the MAOA gene is not predictive of antisocial behaviors later in life ([3][3]). Perhaps Cohen found it amusing that Venter's genome supposedly predicted risk for antisocial behavior. However, the misinformation spread by such mistakes, or premature conclusions regarding behavioral genetics research, could result in much more damaging consequences for other individuals whose genomes are sequenced, especially if they are not in as secure a position as Dr. Venter. 1. 1.[↵][4]1. S. Levy 2. et al. , PLoS 5, 10 (2007). [OpenUrl][5][CrossRef][6][Web of Science][7] 2. 2.[↵][8]1. A. Caspi 2. et al. , Science 297, 851 (2002). [OpenUrl][9][Abstract/FREE Full Text][10] 3. 3.[↵][11]1. C. Morris 2. et al. , GeneWatch 20, 2 (2007). [OpenUrl][12] [1]: #ref-1 [2]: #ref-2 [3]: #ref-3 [4]: #xref-ref-1-1 View reference 1. in text [5]: {openurl}?query=rft.jtitle%253DPLoS%26rft.volume%253D5%26rft.spage%253D10%26rft.atitle%253DPLOS%26rft_id%253Dinfo%253Adoi%252F10.1371%252Fjournal.pbio.0050010%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [6]: /lookup/external-ref?access_num=10.1371/journal.pbio.0050010&link_type=DOI [7]: /lookup/external-ref?access_num=000245243100002&link_type=ISI [8]: #xref-ref-2-1 View reference 2. in text [9]: {openurl}?query=rft.jtitle%253DScience%26rft.stitle%253DScience%26rft.aulast%253DCaspi%26rft.auinit1%253DA.%26rft.volume%253D297%26rft.issue%253D5582%26rft.spage%253D851%26rft.epage%253D854%26rft.atitle%253DRole%2Bof%2BGenotype%2Bin%2Bthe%2BCycle%2Bof%2BViolence%2Bin%2BMaltreated%2BChildren%26rft_id%253Dinfo%253Adoi%252F10.1126%252Fscience.1072290%26rft_id%253Dinfo%253Apmid%252F12161658%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [10]: /lookup/ijlink/YTozOntzOjQ6InBhdGgiO3M6MTQ6Ii9sb29rdXAvaWpsaW5rIjtzOjU6InF1ZXJ5IjthOjQ6e3M6ODoibGlua1R5cGUiO3M6NDoiQUJTVCI7czoxMToiam91cm5hbENvZGUiO3M6Mzoic2NpIjtzOjU6InJlc2lkIjtzOjEyOiIyOTcvNTU4Mi84NTEiO3M6NDoiYXRvbSI7czoyNToiL3NjaS8zMTgvNTg1Ni8xNTUwLjEuYXRvbSI7fXM6ODoiZnJhZ21lbnQiO3M6MDoiIjt9 [11]: #xref-ref-3-1 View reference 3. in text [12]: {openurl}?query=rft.jtitle%253DGeneWatch%26rft.volume%253D20%26rft.spage%253D2%26rft.atitle%253DGENEWATCH%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx