L1 retrotransposons have been replicating and evolving in mammalian species since ≥ 80 million years ago. Novel L1 families repeatedly arose, only to go extinct coincident with the emergence of another novel L1 family. This pattern has persisted to the present despite the fact that L1 activity is deleterious to its host.

The pattern of mammalian L1 evolution resembles that of the influenza virus HA antigen in humans. The latter is explained by the successive emergence of viral variants that bypass existing host defenses (immunity) followed by the reestablishment of host immunity. We suggest that an analogous adversarial interaction between L1 and its host could explain the pattern of L1 evolution.

Projects that examine the interaction of L1 and its host:

- Determine host factors that interact with regions of L1 that have been either highly conserved or undergone adaptive evolution.

- Analysis of the structural and functional consequences of adaptive changes undergone by L1 encoded proteins.

Ongoing projects also include the use of L1 DNA "fossils" generated by now extinct L1 families to examine the history and architecture of the mammalian genome.

Additional information and references can be found at http://www.niddk.nih.gov/intram/people/afurano.htm.

AVAILABILITY: Winter, 2008

QUALIFICATIONS & APPLICATION:

Applicants must have received a doctoral degree within the last 5 years.

Demonstrated proficiency in molecular biology and biochemistry, and a working knowledge of bioinformatics, the Unix operating system, and computer languages (preferably Perl) are essential.

Applicants may apply online (preferred) or e-mail their CV & Bibliography, a short description of research interests, and contact information (including e-mail address and telephone number) for three references to Anthony V. Furano: avf@helix.nih.gov.


The NIH is dedicated to building a diverse community in its training and employment programs.

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