Endoreduplication in Arabidopsis thaliana: control mechanisms and its effect on tolerance towards environmental stresses

Endoreduplication is a widespread phenomenon during which the DNA is re-replicated without mitosis phase. Many roles have been proposed for endoreduplication, including metabolism activity, plant growth or development and environmental adaptation. Endoreduplication responds to many different factors, such as hormones and environmental conditions, and is under the control of many cell cycle-related genes. Recently, the E2Fe/DEL1 gene was shown to be a negative regulator of the cell-cycle-to-endoreduplication transition. Thus the role of the members of the DEL family on endoreduplication was investigated. Overexpression of E2Ff/DEL3 led to an endoreduplication augment in leaves while E2Fd/DEL2 seemed to have no effect on DNA endoreplication. While typical E2Fs interplay and are able to activate atypical E2Fs, atypical E2Fs seem unable to activate or repress other E2Fs. Through their effect on cell cycle genes activity and expression, hormones can have an impact on endoreduplication levels. Phytosterols and brassinosteroids are synthesized from identical start compounds, and have distinct effects on plant physiological development. Both components are important for cell division, while only brassinosteroids are seemingly involved in the control of cell size. Fenpropimorph, a drug inhibiting the synthesis of phytosterols and brassinosteroids, was found to severely inhibit leaf expansion, cell expansion and endoreduplication. Interestingly, CDKB1;1.N161 plants presented decreased fenpropimorph sensitivity in terms of ploidy. Cold nights have shown to have an negative impact on endoreduplication extent, cell enlargement and leaf size. The mutants with low and high ploidy levels did not present dramatic differences in growth reduction compared to wild type plants, suggesting that endoreduplication in not conferring any advantage or disadvantage to plants towards cold temperatures conditions. Endoreduplication has been proposed to confer a protection towards DNA-damaging radiations. The E2Fe/DEL1KO mutant plants, displaying increased ploidy levels, performed better after a UV-B treatment, which was primarily due to their increased levels of PHR1, an UV-induced DNA-damage repair enzyme, and only marginally to their elevated ploidy levels. PHR1 was identified as a direct E2Fe/DEL1 target gene. By combining a control on DNA repair mechanisms through PHR1 repression and endoreduplication through CCS52A2 repression, E2Fe/DEL1 may be able to maintain cells in an undifferentiated state.