Abstract
Several genes involved in the regulation of postembryonic organ initiation and growth have been identified. However, it remains largely unclear how developmental cues connect to the cell cycle. RETINOBLASTOMA RELATED (RBR) is a plant homolog of the tumor suppressor Retinoblastoma (pRb), which is a key regulator of the cell cycle. Using inducible RNA interference (RNAi) against Arabidopsis thaliana RBR (RBRi), we reduced RBR expression levels at different stages of plant development. Conditional reduction or loss of RBR function disrupted cell division patterns, promoted context-dependent cell proliferation, and negatively influenced establishment of cell differentiation. Several lineages of toti- and pluripotent cells, including shoot apical meristem stem cells, meristemoid mother cells, and procambial cells, failed to produce appropriately differentiated cells. Meristem activity was altered, leading to a disruption of the CLAVATA-WUSCHEL feedback loop and inhibition of lateral organ formation. Release of RBR from RNAi downregulation restored meristem activity. Gene profiling analyses soon after RBRi induction revealed that a change in RBR homeostasis is perceived as a stress, even before genes regulated by RBR-E2F become deregulated. The results establish RBR as a key cell cycle regulator required for coordination of cell division, differentiation, and cell homeostasis.
Highlights
Retinoblastoma (RB) was the first tumor suppressor gene identified in animals (Friend et al, 1986) and later was associated with cell cycle regulation, establishing pRb as a key regulator of cell proliferation
RETINOBLASTOMA RELATED (RBR) protein levels could be effectively manipulated in DEX-inducible plants, the GVG-induced phenotypes may obscure or amplify phenotypes produced by deregulation of RBR expression
The construction of an inducible RBRi system allowed us to reduce RBR levels rapidly and transiently, in the absence of confounding effects that may be associated with downregulation of RBR expression by virus-induced gene silencing (VIGS) (Park et al, 2005; Jordan et al, 2007) or expression of plant virus proteins that interact with RBR (Desvoyes et al, 2006; Lageix et al, 2007)
Summary
Retinoblastoma (RB) was the first tumor suppressor gene identified in animals (Friend et al, 1986) and later was associated with cell cycle regulation, establishing pRb as a key regulator of cell proliferation. It is widely accepted that mitogenic signals activate several cyclin-dependent kinase (CDK)-cyclin complexes during progression through G1 to phosphorylate pRb, thereby releasing it from interactions with E2F/DP transcription factor complexes to facilitate S-phase entry (Weinberg, 1995). PRb was found to regulate tissue-specific transcription factors that regulate cell differentiation, such as MyoD, which activates muscle-specific genes (De Falco et al, 2006). Together with the tumor suppressor p53, pRb regulates adipocyte differentiation and function (Hallenborg et al, 2009). The loss of RB function in cardioblasts affects cell differentiation by modulating the activity of cardiogenic factors (Papadimou et al, 2005)
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