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Desvoyes, B.

Publications and source records attributed to Desvoyes, B..

4 recordsLinked to original sources

The Arabidopsis SHORTROOT network coordinates shoot apical meristem development with auxin dependent lateral organ initiation

Unlike animals, plants have the capacity to produce new organs post-embryonically throughout their entire life cycle. This is due to stem cells present in the shoot and the root apical meristems (SAM and RAM, respectively). In the SAM, stem cells are located in the central zone (CZ) where they divide slowly. Stem cell daughters are displaced laterally and enter the peripheral zone (PZ). Here, their mitotic activity increases, and lateral organ primordia (LOP) are formed. How the spatial arrangement of these different domains is initiated and controlled during SAM growth and development, and how sites of LOP are determined in the PZ is not yet completely understood. In the RAM, the GRAS family transcription factor SHORTROOT (SHR) acts as a master regulator of signalling pathways that maintain the root stem cell niche and control formation of ground tissue layers. We hypothesized that SHR could perform a similar role in the SAM, and found that SHR, together with its target transcription factors SCARECROW (SCR), SCARECROW-LIKE23 (SCL23) and JACKDAW (JKD), controls shoot meristem size by regulating cell division rates, and promotes formation of lateral organs. SHR, SCR, SCL23 and JKD are expressed in very distinct patterns in the SAM. Where these expression domains overlap, they can physically interact to activate expression of the key cell cycle regulator CYCLIND6;1 (CYCD6;1) and thereby promote the formation of new cell layers. In the PZ, upregulation of SHR expression at sites of organ initiation depends on the phytohormone auxin, acting through the auxin response factor MONOPTEROS (MP) and auxin response elements in the SHR promoter. In the CZ, the SHR-target SCL23 physically interacts with WUS, a key regulator of stem cell maintenance, and both SCL23 and WUS expression are subject to negative feedback regulation from stem cells through the CLAVATA signalling pathway. Together, our findings illustrate how SHR-dependent transcription factor complexes act in different domains of the shoot meristem to mediate cell division and auxin dependent organ initiation in the PZ, and coordinate this activity with stem cell maintenance in the CZ of the SAM.

plant biology↗

Stem cell regulators control a G1 duration gradient in the plant root meristem

In meristems, where new plant organs initiate, key stem cell regulators have been identified, but their link to cell cycle progression remains unclear. Here, we show that the root meristem has a positional gradient of G1 duration that ranges from [~]2 h near the meristem boundary to more than 20 h in stem cells and early derivatives. Mutants in the PLETHORA (PLT) genes shortened G1 length and flattened its gradient. Computer modeling of an incoherent feed-forward loop (IFFL) predicted the inference of a negative regulatory pathway. We propose that PLT genes play opposing roles, maintaining meristem and stem cell activity and inhibiting G1 progression through the CDK inhibitor KRP5, a PLT target, and RBR1. This establishes a previously undescribed proximal-distal feature of the root meristem in which a G1 duration gradient is shaped by stem cell and meristem maintenance regulators.

plant biology↗

The Polycomb group protein MEDEA controls cell proliferation and embryonic patterning in Arabidopsis

Establishing the body plan of a multicellular organism relies on precisely orchestrated cell divisions coupled with pattern formation. In animals, cell proliferation and embryonic patterning are regulated by Polycomb group (PcG) proteins that form various multisubunit complexes (Grossniklaus and Paro, 2014). The evolutionary conserved Polycomb Repressive Complex 2 (PRC2) trimethylates histone H3 at lysine 27 (H3K27me3) and comes in different flavors in the model plant Arabidopsis thaliana (Forderer et al., 2016; Grossniklaus and Paro, 2014). The histone methyltransferase MEDEA (MEA) is part of the FERTILIZATION INDEPENDENT SEED (FIS)-PRC2 required for seed development4. Although embryos derived from mea mutant egg cells show morphological abnormalities (Grossniklaus et al., 1998), defects in the development of the placenta-like endosperm are considered the main cause of seed abortion (Kinoshita et al., 1999; Scott et al., 1998), and a role of FIS-PRC2 in embryonic patterning was dismissed (Bouyer et al., 2011; Leroy et al., 2007). Here, we demonstrate that endosperm lacking MEA activity sustains normal embryo development and that embryos derived from mea mutant eggs abort even in presence of a wild-type endosperm because MEA is required for embryonic patterning and cell lineage determination. We show that, similar to PcG proteins in mammals, MEA regulates embryonic growth by repressing the transcription of core cell cycle components. Our work demonstrates that Arabidopsis embryogenesis is under epigenetic control of maternally expressed PcG proteins, revealing that PRC2 was independently recruited to control embryonic cell proliferation and patterning in animals and plants.

developmental biology↗

FBL17 targets CDT1a for degradation in early S-phase to prevent Arabidopsis genome instability

Maintenance of genome integrity depends on controlling the availability of DNA replication initiation proteins, e.g., CDT1, a component of the pre-replication complexes that regulates chromatin licensing for replication. To understand the evolutionary history of CDT1 regulation, we have identified the mechanisms involved in CDT1 dynamics. During cell cycle, CDT1a starts to be loaded early after mitotic exit and maintains high levels until the G1/S transition. Soon after the S-phase onset, CDT1a is rapidly degraded in a proteasome-dependent manner. Plant cells use a specific SCF-mediated pathway that relies on the FBL17 F-box protein for CDT1a degradation, which is independent of CUL4a-containing complexes. A similar oscillatory pattern occurs in endoreplicating cells, where CDT1a is loaded just after finishing the S-phase. CDT1a is necessary to maintain genome stability, an ancient strategy although unique proteins and mechanisms have evolved in different eukaryotic lineages to ensure its degradation during S-phase.\n\nImpact statementThe DNA replication protein CDT1a is crucial for genome integrity and is targeted for proteasome degradation just after S-phase initiation by FBL17 in proliferating and endoreplicating cells of Arabidopsis

plant biology↗