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1. Mist and replication

   https://doi.org/10.1038/s41567-022-01549-4  

   Rajamani, Sudha; Biondi, Elisa (May 2022, Nature Physics)
2. Repression of turnip crinkle virus replication by its replication protein p88

   Zhang, S; Sun, R; Guo, Q; Zhang, X-F; Qu, F (January 2019, Virology)

   We recently reported that p28, one of the two turnip crinkle virus (TCV) replication proteins, trans-complemented a defective TCV lacking p28, yet repressed the replication of another TCV replicon encoding wildtype p28 (Zhang et al., 2017). Here we show that p88, the TCV-encoded RNA-dependent RNA polymerase, likewise trans-complemented a p88-defective TCV replicon, but repressed one encoding wild-type p88. Surprisingly, lowering p88 protein levels enhanced trans-complementation, but weakened repression. Repression by p88 was not simply due to protein over-expression, as deletion mutants missing 127 or 224 N-terminal amino acids accumulated to higher levels but were poor repressors. Finally, both trans-complementation and repression by p88 were accompanied by preferential accumulation of subgenomic RNA2, and a novel class of small TCV RNAs. Our results suggest that repression of TCV replication by p88 may manifest a viral mechanism that regulates the ratio of genomic and subgenomic RNAs based on p88 abundance. 

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3. Repression of turnip crinkle virus replication by its replication protein p88

   https://doi.org/doi.org/10.1016/j.virol.2018.10.024  

   Zhang, S.; Sun, R.; Guo, Q.; Zhang, X.-F.; Qu, F. (January 2019, Virology)

   We recently reported that p28, one of the two turnip crinkle virus (TCV) replication proteins, trans-complemented a defective TCV lacking p28, yet repressed the replication of another TCV replicon encoding wildtype p28 (Zhang et al., 2017). Here we show that p88, the TCV-encoded RNA-dependent RNA polymerase, likewise trans-complemented a p88-defective TCV replicon, but repressed one encoding wild-type p88. Surprisingly, lowering p88 protein levels enhanced trans-complementation, but weakened repression. Repression by p88 was not simply due to protein over-expression, as deletion mutants missing 127 or 224 N-terminal amino acids accumulated to higher levels but were poor repressors. Finally, both trans-complementation and repression by p88 were accompanied by preferential accumulation of subgenomic RNA2, and a novel class of small TCV RNAs. Our results suggest that repression of TCV replication by p88 may manifest a viral mechanism that regulates the ratio of genomic and subgenomic RNAs based on p88 abundance. 

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4. More Than One Replication Study Is Needed for Unambiguous Tests of Replication

   https://doi.org/10.3102/1076998619852953  

   Hedges, Larry V.; Schauer, Jacob M. (June 2019, Journal of Educational and Behavioral Statistics)

   The problem of assessing whether experimental results can be replicated is becoming increasingly important in many areas of science. It is often assumed that assessing replication is straightforward: All one needs to do is repeat the study and see whether the results of the original and replication studies agree. This article shows that the statistical test for whether two studies obtain the same effect is smaller than the power of either study to detect an effect in the first place. Thus, unless the original study and the replication study have unusually high power (e.g., power of 98%), a single replication study will not have adequate sensitivity to provide an unambiguous evaluation of replication. 

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5. The Statistics of Replication

   https://doi.org/10.1027/1614-2241/a000173  

   Hedges, Larry V. (October 2019, Methodology)

   Abstract. The concept of replication is fundamental to the logic and rhetoric of science, including the argument that science is self-correcting. Yet there is very little literature on the methodology of replication. In this article, I argue that the definition of replication should not require underlying effects to be identical, but should permit some variation in true effects to be allowed. I note that different possible analyses could be used to determine whether studies replicate. Finally, I argue that a single replication study is almost never adequate to determine whether a result replicates. Thus, methodological work on the design of replication studies would be useful. 

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