C1/P4.20Lateral root emergence: A paradigm for cell signaling in plants

B.Peret (UniversityofNottingham); L. Laplaze (IRD);R. Swarup (Universityof Nottingham); M.J. Bennett (University of Nottingham)

Lateral roots originate deep within the parental root from a smallnumberof foundercells at theperipheryof thevascular tissues andmustemerge through intervening layers of tissues. Despite its importance tothe integrity of the root system, little is known about the regulation oflateral root emergence.Our study reveals that lateral root emergence is ahighly regulated process involving the active participation of cells inboth new lateral root primordia and the parental root. The hormoneauxin originating from the developing lateral root appears to act as alocal inductive signal which reprograms adjacent cells. Auxin inducesthe expression of a previously uncharacterized auxin influx carrier LAX3in cortical and epidermal cells directly overlaying new primordia.Increased LAX3 activity reinforces the auxin-dependent induction of aselection of cell wall remodelling enzymes, promoting cell separation inadvance of developing lateral root primordia.

doi:10.1016/j.cbpa.2008.04.359

C1/P4.21Signalling in the Arabidopsis root meristem

K. Lindsey (Durham University); S. Casson, (University of Bristol); J.Topping (Durham University)

The patterning andmaintenance of the root meristem in Arabidopsisis the consequence of interactions between hormones and overlappingtranscription factors. Radial pattern is established by interactionsbetween SCARECROW (SCR) and SHORT-ROOT (SHR), both membersof the GRAS transcription factor family. Both SCR and SHR proteins arealso found in thequiescent centre (QC), a groupof slowlydividing cells inthemeristem that play a critical role inmaintaining the undifferentiatedstate of the surrounding stem cells. The distribution of auxin by theAUX1andPINproteins is essential tomaintainpattern. The transcriptionfactors PLETHORA1 and 2 (PLT1 and 2) are activated by auxin in the QCand in the surrounding stem cell niche, overlapping with SCR and SHR.plt1 plt2 double mutants cannot specify the QC and so cannot maintainstemcell identity. This is consistentwith amodel for a combinatorial rolefor these transcription factors in controlling stem cell identity andactivity in the root meristem, and in response to auxin. Here we willdescribe the analysis of the STL1 gene, a novel gene in Arabidopsis. STL1expression initiates early in embryogenesis and was identified usinglaser-capture microdissection and microarray analysis of developingembryos. It is required for both the correct patterning of the embryo androot meristem but also maintenance of meristem activity. STL1 activityappears to be independent of PLTgene activity and auxin but is requiredto establish a correct auxin maximum and PLT gene expression.

doi:10.1016/j.cbpa.2008.04.360

C1/P4.22Signalling to programmed cell death in self-incompatible pollen

M. Bosch, B. de Graaf, N. Poulter, S. Vatovec, S. Li, V. Franklin-Tong(University of Birmingham)

Many higher plants use self incompatibility (SI) to prevent self-fertilization. In Papaver rhoeas, the rejection of “self” pollen involvesa Ca2+-dependent signalling network that triggers programmedcell death (PCD), providing a neat way to get rid of unwantedincompatible (“self”) pollen. Several SI-induced events have beenidentified, including: rapid depolymerization of the actin andmicrotubule cytoskeleton (Snowman et al., 2002; Poulter et al.,2008); phosphorylation of a soluble inorganic pyrophosphatase(Rudd et al., 1996; de Graaf et al., 2006); activation of a MAPK, p56(Rudd et al., 2003; Li et al., 2007), and PCD, which involves severalcaspase-like activities, including a DEVDase, VEIDase and a LEVDase(Bosch and Franklin-Tong, 2007; Thomas and Franklin-Tong, 2004).PCD provides a precise mechanism for the specific destruction of“self” pollen. Our focus recently has been on beginning to attempt tounderstand how the signalling networks involved in SI-mediatedPCD are integrated. I will present recent data providing evidence foractin, microtubules and MAPK signalling to activate caspase-likeactivities, resulting in PCD.

References

Snowman, B.N., Kovar, D.R., Shevchenko, G., Franklin-Tong, V.E.,Staiger, C.J., 2002. Plant Cell 14, 2613–2626 2002.

Poulter, N.S., Vatovec, S., Franklin-Tong, V.E., 2008. Plant Physiol. 146,1358–1367.

Rudd, J.J., Franklin, F.C.H., Lord, J.M., Franklin-Tong, V.E., 1996. PlantCell 8, 713–724.

de Graaf, B.H.J., Rudd, J.J., Wheeler, M.J., Perry, R.M., Bell, E.M., Osman,K., Franklin, F.C.H., Franklin-Tong, V.E., 2006. Nature 444, 490–493.

Rudd, J.J., Osman, K., Franklin, F.C.H., Franklin-Tong, V.E., 2003. FEBSLett. 547, 223–227.

Li, S., Samaj, J., Franklin-Tong, V.E., 2007. Plant Physiol. 145, 236–245.Bosch, M., Franklin-Tong, V.E., 2007. PNAS USA 104, 18327–18332.Thomas, S.G., Franklin-Tong, V.E., 2004. Nature 429, 305–309.

doi:10.1016/j.cbpa.2008.04.361

C1/P4.23Control of stomatal development

J. Gray, L. Hunt (University of Sheffield)

Stomata are pores on the aerial surfaces of plants that facilitate theexchange of CO2 and water vapour with the environment. Each pore isformed by a pair of guard cellswhich expand and contract in response toenvironmental signals, to control pore aperture and water loss. Thenumber of stomata that develop on the leaf surface is also underenvironmental control with, for example, less stomata being formed onplants grown at elevated CO2 levels. Studies of Arabidopsis thalianamutants have identified a number of genes controlling thepattern of celldivisions leading to stomatal formation and patterning. From analysis ofplants with altered expression of these genes it appears that anextracellular signaling pathway involving peptides and processingproteases in combination with LRR receptor complexes activate anintracellularMAPK cascade that inhibits entry to the stomatal lineage byrestricting the formation and division of meristemoids. Recent resultssuggesting that secretory peptides, expressed early in leaf development,limit the capacity of cells to enter the stomatal lineagewill be discussed.

doi:10.1016/j.cbpa.2008.04.362

S144 Abstracts / Comparative Biochemistry and Physiology, Part A 150 (2008) S139–S147