Abstract
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 up-regulated during flagellar regeneration in Chlamydomonas, and this up-regulation is critical for flagella to reach their final length, but it not known how the cell triggers these genes during regeneration. We present two models based on transcriptional repressor that is produced either in the flagellum or in the cell body and sequestered in the growing flagellum. Both models lead to stable flagellar length control and can reproduce the observed dynamics of 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 the heterotrimeric 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. Inhibiting axonemal assembly has a much smaller effect on gene expression. The repressor sequestration model allows precursor production to occur when flagella are growing rapidly, representing a form of derivative control.