Endoreduplication is controlled by both external and internal signals, and one of the most established environmental signals that affect the endocycle in plants is light. The growth of Arabidopsis hypocotyls is light-dependent, i.e. in the dark they etiolate and form long and thin hypocotyls whereas in the light they form short and thick hypocotyls (Fig. 1A). Regardless of the light condition where seedlings are grown, these hypocotyls are composed of approximately 22 cells along their longitudinal axis and their growth is primarily driven by cell expansion rather than cell division. This growth is associated with an increase in ploidy up to 16C in the light and to 32C in the dark (Gendreau et al. 1997, Fig. 1A). PHYTOCHROMEB (PHYB) encodes a photoreceptor to absorb red light, and hypocotyls from its loss-of-function mutants display etiolated growth in the light. This phenotype is accompanied by an increase in ploidy (Gendreau et al. 1998), suggesting that PHYB-mediated red light signalling is involved in the control of endoreduplication. Interestingly, mutations in a blue light receptor CRYPTOCHROME 1 (CRY1) also lead to the etiolated hypocotyl phenotype in the light but these mutations have only minor effects on the endocycle (Gendreau et al. 1998). Therefore, the mechanism that suppresses hypocotyl elongation in the light appears to involve at least two genetic pathways, i.e. one that is endocycle dependent and mediated by red light and another that is endocycle independent and mediated by blue light.
What are the downstream signals that transduce these light signals to control the endocycle? One strong candidate that might be involved in this light signalling is CONSTITUTIVELY PHOTOMORPHOGENESIC 1 (COP1), a negative regulator of general light signalling in Arabidopsis because both hypocotyl elongation and endoreduplication is suppressed in cop1 mutants (Gendreau et al. 1998). Another candidate gene that is likely to be involved in these signalling cascades is INCREASED POLYPLOIDY LEVEL IN DARKNESS 1-1D (IPD1-1D) that encodes a plant-specific protein with unknown function (Tsumoto et al. 2006). The ipd1-1D mutant was identified as an over-endoreduplicated hypocotyl mutant from activation tagging lines. Interestingly, ipd1-1D mutants only display the ploidy phenotype in the dark and in agreement with this, IPD1 is transcriptionally down regulated by light. Part of the IPD1 protein is homologous to the CUE domain which is required for binding to mono ubiquitin, suggesting that IPD1 may target some negative regulator of the endocycle for protein modification. However, the CUE domain within IPD1 lacks a well-conserved amino acid that is essential for its binding to mono ubiquitin. Therefore, it is possible that IPD1 has some unrelated function in regulating the endocycle and hypocotyl elongation through light signalling.
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