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How bio-membranes are self-organized to perform their functions remains a pivotal issue in biological and chemical science. Understanding the self-assembly principles of lipid-like molecules hence becomes crucial. Here we report the meso-structural evolution of amphiphilic sphere-rod conjugates (giant lipids), and study the roles of geometric parameters (head-tail ratio and cross-section area) during this course. As a prototype system, giant lipids resemble natural lipidic molecules by capturing their essential features including head-tail configuration, monodispersed molecular weight distribution and minor interpenetration of hydrophobic tails. We demonstrate the self-assembly behavior of two categories of giant lipids (I-shape and T-shape, a total of 8more »
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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 andmore »
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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 andmore »
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