The effect of the <i>clv3</i> mutation on WUS expression.

<p>Green shows the extent of WUS expression in wildtype, and red shows WUS expression in the clv3 mutant. The expression zones are defined as cells that express WUS at the half maximum level of expression in the mutant or higher. In the mutant the concentration of WUS increases, this means the number of cells that express WUS at a high enough level to be considered within the expression zone, increases. For examples of models out put in an uncropped template see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0147830#pone.0147830.s002" target="_blank">S2 Fig</a>.</p

SAM architecture and its representation in the model.

<p>(A) An image of the SAM and the immediate surrounding area. The regions of interest are marked with colored boundaries. (B) Schematic representation of WUS and CLV domains; the three dimensional SAM, consisting of cells of various shapes and sizes, is modeled by a two dimensional grid consisting of identical blocks representing cells. The field of cells extend farther in lateral and basal directions. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0147830#pone.0147830.s002" target="_blank">S2 Fig</a> depicts the complete cellular template used for simulations.</p

Extension of L1 signal beyond the first three cell layers.

<p>The white bar in the figures show the distance at which the concentration of the L1 signal drops to 10% of its initial concentration (A) CLV3 expression in wt. (B) CLV3 expression resulting from the extended L1 signal. the CLV3 mRNA expression extends to organizing center. This has never been observed experimentally in the wildtype SAM, hence the model predict that L1 signal is confined to the upper three cell layers. For examples of models out put in an uncropped template see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0147830#pone.0147830.s002" target="_blank">S2 Fig</a>.</p

Wildtype expression pattern of the molecules in the model.

<p>The relative levels in each figure are depicted by a color spectrum shown by the color bar in the figure. For examples of models out put in an uncropped template see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0147830#pone.0147830.s002" target="_blank">S2 Fig</a>.</p

Two coupled sub-networks and boundary information define WUS and CLV3 expression domains in the SAM.

<p><i>A</i> and <i>B</i> stand for type-b and type-A ARRs. <i>A</i>_<i>p</i> and <i>B</i>_<i>p</i> denote phosphorylated type-B and type-B ARRs. (A) The model can be divided into the CK signaling (blue) and WUS/CLV3 (green) sub-networks combined with boundary morphogens (L1 and CK). The former determines the position of the WUS domain via a self-organizing system while the latter specifies the CLV3 domain, taking the WUS domain as an input. The network consists of interactions and molecules that are based on published experimental data (black arrows and letters) and hypothetical interactions and molecules (red arrows and letters). Parts of the CK signaling sub-network correspond to the components of the (B) classical activator/inhibitor system; (C) the network component corresponding to the autocatalytic activator and (D) to the activation/inhibition interactions.</p

WUS and CLV3 expression patterns after <i>in silico</i> ablation.

<p>(A) and (C): the wildtype expression pattern of WUS and CLV3. (B) and (D): WUS and CLV3 expression patterns that form after ablation of the center of the SAM including the SCD and OC. For examples of models out put in an uncropped template see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0147830#pone.0147830.s002" target="_blank">S2 Fig</a>.</p

Laser ablation of <i>WUS</i>, <i>CLV3</i> and <i>TCS</i> domains.

<p><i>WUS::GFP</i> promoter fusion expression before (A), just after (B) and 1 d after (C) laser ablation. <i>CLV3::GFP</i> expression before (D), just after (E) and 1 d after (F) laser ablation. <i>TCS</i> promoter expression before (G), just after (H) and 2 d (I) after laser ablation. The green signal is <i>WUS::GFP</i> in A, B, C, <i>CLV3::GFP</i> in D, E, F, <i>TCS</i> in G, H, I. Red signal is propidium-iodide (PI)-stained cell wall or laser ablated cells.</p

CK lifetime as a function of <i>D</i>_<i>eff</i> and <i>n</i>₀.

<p>The average lifetime <i>τ</i> of CK in minutes in the meristem and the extension <i>n</i>₀ in cell layers of the CK synthesis zone consistent with the observation of a CK profile covering the upper 25 cell layers of the meristem. The colorbar shows the chosen value of the effective diffusion constant of CK in the meristemic tissue, ranging from 42<i>μm</i>² <i>s</i>⁻¹ to 241<i>μm</i>² <i>s</i>⁻¹ (see text).</p

MOESM7 of Boosting LPMO-driven lignocellulose degradation by polyphenol oxidase-activated lignin building blocks

Additional file 7: Table S2. Selected cellulase-rich Ascomycota from the JGI database1

MOESM1 of Boosting LPMO-driven lignocellulose degradation by polyphenol oxidase-activated lignin building blocks

Additional file 1: Figure S1. Activity of MtLPMO9B towards amorphous cellulose in the presence and absence of MtPPO7 or AbPPO. HPAEC elution pattern of regenerated amorphous cellulose (RAC; 1.5 mg mL−1) incubated with MtLPMO9B (red, 5.0 μg mL−1) only, or with either AbPPO (blue, 2.5 µL mL−1) or MtPPO7 (yellow, 5.0 μg mL−1) in the presence of (a) para-coumaric acid (no. 3 specified in Table 1, 2 mM) and (b) 3-hydroxy-4-methoxycinnamic acid (no. 5 specified in Table 1, 2 mM). The incubation of RAC with MtLPMO9B results in the formation of non-oxidized gluco-oligosaccharides (GlcOSn) and C1-oxidized gluco-oligosaccharides (GlcOS n # ). See “Methods” for details