E2Fc AND E2Fb TRANSCRIPTION FACTORS INDEPENDENTLY REGULATE PLANT GROWTH UNDER UV-B CONDITIONS IN ARABIDOPSIS THALIANA

MARÍA SOL GOMEZ; MARÍA DEL LUJAN SHERIDAN; MARÍA LORENA FALCONE-FERREYRA; PAULA CASATI

Congreso; 2019 ESP-IUPB World Congress; 2019

UV-B radiation inhibits plant growth, and this inhibition is, to a certain extent, regulated by the activity of the E2Fetranscription factor. E2Fe is a target of regulation by two transcription factors from the same family, E2Fb and E2Fc.While E2Fc acts as a repressor, E2Fb is a transcriptional activator of E2Fe. Therefore, we investigated if the modulationof UV-B responses by E2Fe is through its regulation by E2Fb and/or E2Fc. We found that, at UV-B intensities thatinduce DNA damage, inhibition of cell proliferation is regulated by both E2Fc and E2Fb. E2Fc controls leaf size underUV-B regulating DNA damage responses, as E2Fc deficient plants show decreased programmed cell death in theroots after exposure and altered SOG1 and ATR expression. Moreover, E2Fc has an epistatic role over the miR396pathway under UV-B, which also regulates leaf growth under these conditions. On the other hand, although E2Fbalso controls cell proliferation under UV-B conditions; it does not regulate programmed cell death in the roots afterexposure. Interestingly, E2Fb deficient leaf cells have increased DNA ploidy levels after UV-B exposure, similarly asE2Fe deficient cells. Together, our results demonstrate that E2Fc is required for miR396 activity on cell proliferationunder UV-B, and that its role is independent of E2Fe, probably modulating DNA damage responses through theregulation of SOG1 and ATR levels. On the contrary, the regulation of DNA ploidy in leaf cells under UV-B previouslydescribed in E2Fe deficient plants could be regulated by E2Fb activity.