E2FB Interacts with RETINOBLASTOMA RELATED and Regulates Cell Proliferation during Leaf Development

Erika Őszi, Csaba Papdi, Binish Mohammed, Aladár Petkó-Szandtner, Tünde Leviczky, Eszter Molnár, Carlos Galvan-Ampudia, Khan Safina, Enrique Lopez Juez, Beatrix Horvath, Laszlo Bogre, Zoltán Magyar

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Cell cycle entry and quiescence are regulated by the E2F transcription factors in association with the RETINOBLASTOMA-RELATED (RBR). E2FB is considerred to be a transcriptional activator of cell cycle genes, but its function during development is less established. By studying E2FB-RBR interaction, E2F target gene expression, epidermal cell number and shape in e2fb mutant and overexpression lines during leaf development we show that E2FB in association with RBR has roles to inhibit cell proliferation and to establish quiescence. In young leaves both RBR and E2FB are abundant and form a repressor complex that is reinforced by an autoregulatory loop. Increased E2FB level either in its own domain, or ectopically together with DPA, further elevates the amount of this repressor complex, leading to reduced cell number in leaves. That RBR repression specifically acts through E2FB is strongly suggested by the overproliferation in the e2fb mutants and in a line where a truncated form of E2FB, lacking the RBR binding domain, was overexpressed. The increased number of small cells with size below the guard cells and of fully developped stomata provide some evidence that meristemoids preferentially hyperproliferate. As leaf development progresses and cells exit into differentiation, the amount of RBR and E2FB gradually decline. At this stage an elevated E2FB level can escape from RBR repression leading to the reactivation of cell division in pavement cells. In summary, E2FB in association with RBR is central to keep cell proliferation under control during organ development to determine the final cell number.
Original languageEnglish
Pages (from-to)518-533
Number of pages16
JournalPlant physiology
Issue number1
Early online date6 Nov 2019
Publication statusPublished - 6 Jan 2020

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