![]() Perelson, A.S., Neumann, A.U., Markowitz, M., Leonard, J.M. Expansion and contraction of HIV-specific CD4 T cells with short bursts of viremia, but physical loss of the majority of these cells with sustained viral replication. Seth, N., Kaufmann, D., Lahey, T., Rosenberg, E.S. Noise in gene expression determines cell fate in Bacillus subtilis. An excitable gene regulatory circuit induces transient cellular differentiation. Suel, G.M., Garcia-Ojalvo, J., Liberman, L.M. Stochastic kinetic analysis of developmental pathway bifurcation in phage lambda-infected Escherichia coli cells. Multistability in the lactose utilization network of Escherichia coli. Ozbudak, E.M., Thattai, M., Lim, H.N., Shraiman, B.I. ![]() Thus, transcriptional positive feedback can modulate transient expression lifetime to a greater extent than protein half-life modulation, and it has a critical role in the cell-fate decision in HIV. ![]() Notably, artificial weakening of Tat positive feedback shortened the duration of Tat expression transients and biased the probability in favor of latency. By measuring shifts in the autocorrelation of noise inherent to gene expression, we found that transcriptional positive feedback extends the single-cell Tat expression lifetime two- to sixfold for both minimal Tat circuits and full length, actively replicating HIV-1. Here, using an HIV-1 model system, we directly quantify transcriptional feedback strength and its effects on both the duration of HIV-1 Tat transcriptional pulses and the fate of HIV-infected cells. However, transient gene expression has also been proposed to control cell fate 4, 5, with the decision arbitrated by the duration of a transient gene expression pulse. Steady-state behavior and bistability have been proposed as mechanisms for decision making in gene circuits 1, 2, 3.
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