2013 Rustbelt RNA Meeting
RRM
Poster abstracts
Abstract:
Human tRNALys3 serves as the primer for reverse transcription in human immunodeficiency virus type-1 (HIV-1). All tRNALys isoacceptors are selectively packaged into budding virions through specific interactions between human lysyl-tRNA synthetase (hLysRS) and the viral Gag protein. tRNALys3 must be released from hLysRS for annealing to the complementary primer binding site (PBS) in the 5’-UTR of the HIV-1 genome in order to initiate reverse transcription. We have shown that this release is facilitated, in part, by the interaction of hLysRS with a tRNA-like element (TLE) in the HIV-1 genome. In HIV-1 NL4-3, which is a clade B subtype, the TLE is located proximal to the PBS and mimics the U-rich anticodon loop of tRNALys. The goal of this project is to establish the conservation of the TLE across various subtypes of HIV-1. We were particularly interested in investigating the HIV-1 MAL isolate, which is a complex recombinant of clades A, D and I. This isolate is representative of clade A and contains a 20-nt insertion near the PBS, which is known to result in an alternative secondary structure fold of the 5’-UTR. We have used fluorescence anisotropy assays to investigate the binding of hLysRS to MAL-derived RNA constructs. The assays reveal moderate to high affinity binding of hLysRS to MAL 123-218 (a 98-mer RNA containing the PBS; Kd = 413±22 nM) and MAL 123-349 (a 229-mer RNA containing the PBS and the dimer initiation signal, DIS; Kd < 50 nM). To locate the sequence elements responsible for the high-affinity binding, truncated genomic RNAs are being designed and tested. An A-rich 23-nt stem-loop RNA previously shown by NMR to mimic the tRNA anticodon structure showed only weak binding to hLysRS (Kd > 5 uM). The results obtained to date suggest differences in the mechanism of tRNALys3 targeting to the PBS and release from hLysRS in different subtypes of HIV-1.
Keywords: HIV-1, TLE, MAL