| Popis: |
Biosynthesis of organelle precursors is a central part of the organelle size control problem, but what systems are required to control precursor production? Genes encoding flagellar proteins are upregulated during flagellar regeneration in Chlamydomonas, and this upregulation is critical for flagella to reach their final length, but it not known how the cell triggers these genes during regeneration. Here we present two models based on transcriptional repressor that is either produced in the flagellum, or else is produced in the cell body and sequestered in the growing flagellum. We show that both models lead to stable flagellar length control, can reproduce the observed dynamics of gene expression, and are consistent with the effects of protein synthesis inhibitors on gene expression. The two models make opposite predictions regarding the effect of mutations that block intraflagellar transport (IFT). Using quantitative measurements of gene expression, we show that gene expression during flagellar regeneration is greatly reduced in mutations of FLA3, FLA8, and FLA10, which encode the three components of the heterotrimer kinesin-2 that drives IFT. This result is consistent with the predictions of the model in which a repressor is sequestered in the flagellum by IFT. In contrast to the effects of IFT mutants, we find that inhibiting axonemal assembly has much less effect on gene expression, suggesting that transport is more important than axonemal assembly. The repressor sequestration model allows precursor production to occur when flagella are growing rapidly, representing a form of derivative control. |
