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bHLH proteins know when to make a stoma
Update
TRENDS in Plant Science
Vol.12 No.11
Research Focus
bHLH proteins know when to make a stoma Laura Serna Facultad de Ciencias del Medio Ambiente, Universidad de Castilla-La Mancha, E-45071 Toledo, Spain
In Arabidopsis thaliana, stomata develop through a stereotypical pattern of cell divisions. Three recent publications demonstrate that three bHLH proteins act successively in such lineages to drive the formation of stomata. SPEECHLES drives the division that initiates the stomatal-cell lineage. Then MUTE induces the formation of the immediate stomatal precursor cell. Finally, FAMA causes the stomatal precursor cell to divide into the two guard cells that surround each stomatal pore.
How to know how often to divide? Stomata are by far the most influential components in gas exchange. They consist of two guard cells that change shape as a result of turgor pressure; this shape change leads to the opening and closing of the stomatal pore, which, as a result, regulates gas exchange. In Arabidopsis, stomatal development starts with an asymmetric division from an epidermal cell called a meristemoid mother cell [1] (Figure 1). This division yields a triangular meristemoid and a larger cell. Meristemoids can divide asymmetrically up to three more times, and always produce a larger cell and a smaller meristemoid that maintains its stem cell activity. After these asymmetric divisions, the meristemoid loses its stem cell activity and forms a guard mother cell (GMC). The GMC undergoes a symmetric cell division that produces the paired guard cells. The larger cells that result from the asymmetric divisions can divide or become pavement cells. That being said, how does a stomatal precursor cell know how often it should divide before making a stoma? The recent isolation and functional characterization of three members of the basic helix-loop-helix (bHLH) family of transcriptional factors have deepened the mystery [2–4]. Two recent papers have highlighted these findings* [5,6]. Several signalling genes, including STOMATAL DENSITY AND DISTRIBUTION1 (SDD1), TOO MANY MOUTHS (TMM), members of the ERECTA family receptor-like kinases [ERECTA, ERECTA LIKE1 (ERL1) and ERL2], YODA (YDA) and four genes of a MITOGEN-ACTIVATED PROTEIN KINASE (MAPK) signalling module, negatively regulate the development of supernumerary stomata [7–11]. By contrast, the three members of the bHLH family of transcriptional factors promote stomatal development [2–4]. Because these regulators control, in an opposite manner, the same functions (the entrance into the stomatal lineage and/or the stem cell activity of the meristemoids), a Corresponding author: Serna, L. ([email protected]). www.sciencedirect.com
dynamic balance between them must be crucial for stomatal development. SPEECHLESS and MUTE: driving the first and the last asymmetric cell divisions MacAlister et al. found that plants homozygous for the speechless-3 (spch-3) or spch-4 alleles, which lack detectable transcripts, do not develop stomata, and all their epidermal cells consist of jigsaw-puzzle-shaped pavement cells (Figure 2b) [3]. The mutation in spch-1, which eliminates the last seven amino acids of the protein, also induces an identical phenotype. The absence of stomata in these mutants suggests that SPCH drives the division that initiates stomatal development [3]. Supporting such a role, the overexpression of SPCH increases the number of cells entering into the stomatal pathway [3,4]. The missense mutation spch-2 affects the carboxy terminus of the protein, and it reduces the number of stomata [3]. This finding supports the proposed role for SPCH in the regulation for stomatal development and suggests some residual activity of the protein in the spch-2 mutant. In addition, the ability of the spch-2 mutant to develop stomata provides an opportunity to uncover additional functions regulated by the SPCH gene. Based on studies of static pictures of the pedicel epidermis in spch-2, MacAlister et al. concluded that SPCH also maintains the stem cell activity of the meristemoids [3]. The SPCH gene encodes a protein that belongs to the bHLH family of transcription factors [3]. It is expressed in undifferentiated cells and persists in stomatal lineage cells, including guard cells [3]. However, the protein is restricted to early stages of the stomatal lineage, suggesting that the SPCH protein might be downregulated post-transcriptionally [3]. These expression patterns are consistent with a role for SPCH in determination of entrance into the stomatal lineage and, perhaps, a later role in the maintenance of the stem cell activity of the meristemoids, as suggested by the phenotype of spch-2 in the pedicel epidermis. A second bHLH protein, named MUTE and very similar in sequence to SPCH, also controls stomatal development [4]. The loss-of-function mute mutant does not develop stomata but forms meristemoids that abort after excessive asymmetric cell divisions [3,4] (Figure 2c). Both MUTE promoter activity and the MUTE protein are restricted to a subset of meristemoids, with residual activity in GMCs and immature stomata [3,4]. It is therefore probable that, in this subset of meristemoids, MUTE represses stem cell activity and induces GMC formation. The fact that the overexpression of MUTE converts all epidermal cells into
1360-1385/$ – see front matter ß 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.tplants.2007.08.016
484
Update
TRENDS in Plant Science
Vol.12 No.11
Figure 1. SPEECHLESS (SPCH) starts stomatal development by inducing the first asymmetric division, which produces the first meristemoid. Two or three divisions after SPEECHLESS, MUTE drives the last asymmetric cell division causing the formation of the guard mother cell. Then, FAMA drives the symmetric division that gives rise to the two guard cells. The three genes encode bHLH proteins with very similar sequences. Adapted from Refs [3,4].
Figure 2. Epidermal phenotype of wild type (a) and mutants plants (b–d). (a) Wild-type plants develop stomata, (b) which fail to develop in spch mutants. (c) The mute mutant does not develop stomata but forms meristemoids that abort after excessive asymmetric cell divisions. (d) fama lacks mature stomata and, instead, develops clusters of guard mother cells or young guard cells. Adapted from Ref. [3].
stomata is consistent with the role assigned to this gene [3,4]. FAMA and the symmetric division that produces the stoma The FAMA gene encodes a third protein, which belongs to the bHLH family of transcription factors and which is likely to act as a transcriptional activator [2]. Plants homozygous for the insertion mutant fama-1, which have no detectable FAMA transcripts, lack mature stomata and, instead, develop cluster of GMCs or incipient guard cells [2] (Figure 2d). Kyoko Ohashi-Ito and Dominique Bergmann have shown that the induction of the FAMA promoter is restricted to GMCs and young guard cells, and that the FAMA protein localizes to the nucleus of these cells [2]. It is then likely that FAMA causes both the GMC to divide into two guard cells and that it promotes guard cell differentiation. The overexpression of FAMA converts non-stomatal cells to guard cells [2]. These guard cells are not organized into pairs, and it seems that they develop from GMCs that switch to become guard cells without undergoing a symmetrical division [2]. The simplest explanation for these findings is that the activity of FAMA is essential in the regulation of cell division, with high levels repressing cell division and forcing GMCs to differentiate directly into guard cells [2]. Playing downstream of the signalling genes Similarly to the signalling genes (SDD1, TMM, members of the ER-family and YDA), SPCH controls both functions: entrance into the stomatal-cell lineage and the balance between meristemoid renewal and stomatal differentiation, with spch-1 being epistatic to tmm, er, erl1, erl2 and yda mutants [3]. This suggests that SPCH operates downstream of theses genes [3]. In agreement with this view, the overexpression of SPCH driven by its own www.sciencedirect.com
promoter promotes the development of stomata in the hypocotyl of tmm [3], which usually has no stomata. MUTE and the signalling genes control the stem cell fate of the meristemoids, however, they do so in an opposite manner, with MUTE repressing such cell fate and the signalling components inducing it. Like mute, the three mutants mute tmm, mute erecta erl1 erl2 and mute sdd1 do not develop stomata, but the arrangement of the meristemoids is similar to the arrangement of the stomata induced by the mutation(s) in the signalling gene(s) in each case [4]. This suggests that all these genes interact additively [4]. In addition, the absence of stomata in the double or quadruple mutants suggests that MUTE might act downstream of these genes triggering GMC formation [4]. The absence of stomata in mutant combinations between fama and the mutants of the signalling genes ( fama sdd1, fama tmm, fama er erl1 erl2 and fama yda) [2] also places FAMA downstream of such genes with respect to the regulation of guard cell differentiation. Moreover, the arrangement of the GMCs or immature guard cells reflects the phenotype of mutations in the signalling components [2], which suggests that they interact additively with FAMA. In addition to the bHLH regulators of stomatal development, two other proteins belonging to the MYB family of transcription factors have been implicated in this process [12]. Both FOUR LIPS and MYB88 control the formation of the stoma from the GMC [12]. Some MYB proteins regulate transcription by physical interaction with bHLH proteins [13]. However, FOUR LIPS, MYB88 and FAMA do not contain the amino acid signatures defined as necessary for the interaction between MYB and bHLH proteins [6]. Certainly, although several techniques have been used, no interactions between FOUR LIPS or MYB88 and FAMA have been detected [2]. Moreover, neither protein is required for the transcriptional
Update
TRENDS in Plant Science
activation of the other [2]. Together, this suggests that FAMA and FLP/MYB88 control the GMC–guard cell transition independently. Stomatal density is regulated by environmental conditions [14]. Environmental factors that increase stomatal density might be working through the positive regulators (SPCH, MUTE and FAMA). By contrast, those that decrease the number of stomata might be working through the negative ones (SDD1, TMM, ER-family, YDA and the MAPK module). Concluding remarks These results bring us closer to an understanding of how a stomatal precursor knows how often to divide. Among the many challenges that lie ahead is deciphering how SPCH, MUTE and FAMA interact with one another. It would also be interesting to determine not only which genes are regulated by these bHLH proteins, but also how their products function to ensure that fully differentiated stomata develop in the right places. *Note added in proof A new paper covering the same topic has been published during the production of this issue: Pillitteri, L.J. and Torii, K.U (2007) Breaking the silence: three bHLH proteins direct cell-fate decisions during stomatal development. Bioessays 29, 861–870. Acknowledgements I thank C. Martin for critical reading of the manuscript. Work in my laboratory is supported by grants from both the Communities Council of
Vol.12 No.11
485
Castilla-La Mancha (PAI-05–058) and the Ministry of Education and Culture of Spain (BIO2005–04493).
References 1 Bergmann, D.C. and Sack, F.D. (2007) Stomatal Development. Annu. Rev. Plant Biol. 58, 163–181 2 Ohashi-Ito, K. and Bergmann, D.C. (2006) Arabidopsis FAMA controls the final proliferation/differentiation switch during stomatal development. Plant Cell 18, 2493–2505 3 MacAlister, C.A. et al. (2007) Transcription factor control of asymmetric cell divisions that establish the stomatal lineage. Nature 445, 537–540 4 Pillitteri, L.J. et al. (2007) Termination of asymmetric cell division and differentiation of stomata. Nature 445, 501–505 5 Gray, J.E. (2007) Plant development: three steps for stomata. Curr. Biol. 17, R213–R215 6 Barton, M.K. (2007) Making holes in leaves: promoting cell state transitions in stomatal development. Plant Cell 19, 1140–1143 7 Berger, D. and Altmann, T. (2002) A subtilisin-like protease involved in the regulation of stomatal density and distribution in Arabidopsis thaliana. Genes Dev. 14, 1119–1131 8 Nadeau, J.A. and Sack, F.D. (2002) Control of stomatal distribution on the Arabidopsis leaf surface. Science 296, 1697–1700 9 Shpak, E.D. et al. (2005) Stomatal patterning and differentiation by synergistic interactions of receptor kinases. Science 309, 290–293 10 Bergmann, D.C. et al. (2004) Stomatal development and pattern controlled by a MAPKK kinase. Science 304, 1494–1497 11 Wang, H. et al. (2007) Stomatal development and patterning are regulated by environmentally responsive mitogen-activated protein kinases in Arabidopsis. Plant Cell 19, 63–73 12 Lai, L.B. et al. (2005) The Arabidopsis R2R3 MYB proteins FOUR LIPS and MYB88 restrict divisions late in the stomatal lineage. Plant Cell 17, 2754–2767 13 Serna, L. and Martin, C. (2006) Trichomes: different regulatory networks lead to convergent structures. Trends Plant Sci. 11, 274–280 14 Hetherington, A.M. and Woodward, F.I. (2003) The role of stomata in sensing and driving environmental change. Nature 424, 901–908
Symposium Announcement Evolution of Weediness and Invasiveness: Molecular Genetics Approaches February 7, 2008. Hilton Chicago, 720 South Michigan Ave., Chicago, Illinois. A one day symposium and workshop on the use of molecular genomics in weed science will be held in conjunction with the 2008 annual meeting of the Weed Science Society of America, February 4-7, 2008 in Chicago (wssa.net). The symposium portion will feature speakers such as Steve Duke, Jonathan Gressel, Loren Rieseberg, and Rod Wing. Following the complimentary lunch, the workshop portion of the conference will conclude with breakout sessions to discuss and determine the path forward in applying tools from the genomics revolution to weed science. The symposium is organized by Pat Tranel and Neal Stewart. Registration is via the WSSA website (wssa.net). www.sciencedirect.com
TRENDS in Plant Science
Vol.12 No.11
Research Focus
bHLH proteins know when to make a stoma Laura Serna Facultad de Ciencias del Medio Ambiente, Universidad de Castilla-La Mancha, E-45071 Toledo, Spain
In Arabidopsis thaliana, stomata develop through a stereotypical pattern of cell divisions. Three recent publications demonstrate that three bHLH proteins act successively in such lineages to drive the formation of stomata. SPEECHLES drives the division that initiates the stomatal-cell lineage. Then MUTE induces the formation of the immediate stomatal precursor cell. Finally, FAMA causes the stomatal precursor cell to divide into the two guard cells that surround each stomatal pore.
How to know how often to divide? Stomata are by far the most influential components in gas exchange. They consist of two guard cells that change shape as a result of turgor pressure; this shape change leads to the opening and closing of the stomatal pore, which, as a result, regulates gas exchange. In Arabidopsis, stomatal development starts with an asymmetric division from an epidermal cell called a meristemoid mother cell [1] (Figure 1). This division yields a triangular meristemoid and a larger cell. Meristemoids can divide asymmetrically up to three more times, and always produce a larger cell and a smaller meristemoid that maintains its stem cell activity. After these asymmetric divisions, the meristemoid loses its stem cell activity and forms a guard mother cell (GMC). The GMC undergoes a symmetric cell division that produces the paired guard cells. The larger cells that result from the asymmetric divisions can divide or become pavement cells. That being said, how does a stomatal precursor cell know how often it should divide before making a stoma? The recent isolation and functional characterization of three members of the basic helix-loop-helix (bHLH) family of transcriptional factors have deepened the mystery [2–4]. Two recent papers have highlighted these findings* [5,6]. Several signalling genes, including STOMATAL DENSITY AND DISTRIBUTION1 (SDD1), TOO MANY MOUTHS (TMM), members of the ERECTA family receptor-like kinases [ERECTA, ERECTA LIKE1 (ERL1) and ERL2], YODA (YDA) and four genes of a MITOGEN-ACTIVATED PROTEIN KINASE (MAPK) signalling module, negatively regulate the development of supernumerary stomata [7–11]. By contrast, the three members of the bHLH family of transcriptional factors promote stomatal development [2–4]. Because these regulators control, in an opposite manner, the same functions (the entrance into the stomatal lineage and/or the stem cell activity of the meristemoids), a Corresponding author: Serna, L. ([email protected]). www.sciencedirect.com
dynamic balance between them must be crucial for stomatal development. SPEECHLESS and MUTE: driving the first and the last asymmetric cell divisions MacAlister et al. found that plants homozygous for the speechless-3 (spch-3) or spch-4 alleles, which lack detectable transcripts, do not develop stomata, and all their epidermal cells consist of jigsaw-puzzle-shaped pavement cells (Figure 2b) [3]. The mutation in spch-1, which eliminates the last seven amino acids of the protein, also induces an identical phenotype. The absence of stomata in these mutants suggests that SPCH drives the division that initiates stomatal development [3]. Supporting such a role, the overexpression of SPCH increases the number of cells entering into the stomatal pathway [3,4]. The missense mutation spch-2 affects the carboxy terminus of the protein, and it reduces the number of stomata [3]. This finding supports the proposed role for SPCH in the regulation for stomatal development and suggests some residual activity of the protein in the spch-2 mutant. In addition, the ability of the spch-2 mutant to develop stomata provides an opportunity to uncover additional functions regulated by the SPCH gene. Based on studies of static pictures of the pedicel epidermis in spch-2, MacAlister et al. concluded that SPCH also maintains the stem cell activity of the meristemoids [3]. The SPCH gene encodes a protein that belongs to the bHLH family of transcription factors [3]. It is expressed in undifferentiated cells and persists in stomatal lineage cells, including guard cells [3]. However, the protein is restricted to early stages of the stomatal lineage, suggesting that the SPCH protein might be downregulated post-transcriptionally [3]. These expression patterns are consistent with a role for SPCH in determination of entrance into the stomatal lineage and, perhaps, a later role in the maintenance of the stem cell activity of the meristemoids, as suggested by the phenotype of spch-2 in the pedicel epidermis. A second bHLH protein, named MUTE and very similar in sequence to SPCH, also controls stomatal development [4]. The loss-of-function mute mutant does not develop stomata but forms meristemoids that abort after excessive asymmetric cell divisions [3,4] (Figure 2c). Both MUTE promoter activity and the MUTE protein are restricted to a subset of meristemoids, with residual activity in GMCs and immature stomata [3,4]. It is therefore probable that, in this subset of meristemoids, MUTE represses stem cell activity and induces GMC formation. The fact that the overexpression of MUTE converts all epidermal cells into
1360-1385/$ – see front matter ß 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.tplants.2007.08.016
484
Update
TRENDS in Plant Science
Vol.12 No.11
Figure 1. SPEECHLESS (SPCH) starts stomatal development by inducing the first asymmetric division, which produces the first meristemoid. Two or three divisions after SPEECHLESS, MUTE drives the last asymmetric cell division causing the formation of the guard mother cell. Then, FAMA drives the symmetric division that gives rise to the two guard cells. The three genes encode bHLH proteins with very similar sequences. Adapted from Refs [3,4].
Figure 2. Epidermal phenotype of wild type (a) and mutants plants (b–d). (a) Wild-type plants develop stomata, (b) which fail to develop in spch mutants. (c) The mute mutant does not develop stomata but forms meristemoids that abort after excessive asymmetric cell divisions. (d) fama lacks mature stomata and, instead, develops clusters of guard mother cells or young guard cells. Adapted from Ref. [3].
stomata is consistent with the role assigned to this gene [3,4]. FAMA and the symmetric division that produces the stoma The FAMA gene encodes a third protein, which belongs to the bHLH family of transcription factors and which is likely to act as a transcriptional activator [2]. Plants homozygous for the insertion mutant fama-1, which have no detectable FAMA transcripts, lack mature stomata and, instead, develop cluster of GMCs or incipient guard cells [2] (Figure 2d). Kyoko Ohashi-Ito and Dominique Bergmann have shown that the induction of the FAMA promoter is restricted to GMCs and young guard cells, and that the FAMA protein localizes to the nucleus of these cells [2]. It is then likely that FAMA causes both the GMC to divide into two guard cells and that it promotes guard cell differentiation. The overexpression of FAMA converts non-stomatal cells to guard cells [2]. These guard cells are not organized into pairs, and it seems that they develop from GMCs that switch to become guard cells without undergoing a symmetrical division [2]. The simplest explanation for these findings is that the activity of FAMA is essential in the regulation of cell division, with high levels repressing cell division and forcing GMCs to differentiate directly into guard cells [2]. Playing downstream of the signalling genes Similarly to the signalling genes (SDD1, TMM, members of the ER-family and YDA), SPCH controls both functions: entrance into the stomatal-cell lineage and the balance between meristemoid renewal and stomatal differentiation, with spch-1 being epistatic to tmm, er, erl1, erl2 and yda mutants [3]. This suggests that SPCH operates downstream of theses genes [3]. In agreement with this view, the overexpression of SPCH driven by its own www.sciencedirect.com
promoter promotes the development of stomata in the hypocotyl of tmm [3], which usually has no stomata. MUTE and the signalling genes control the stem cell fate of the meristemoids, however, they do so in an opposite manner, with MUTE repressing such cell fate and the signalling components inducing it. Like mute, the three mutants mute tmm, mute erecta erl1 erl2 and mute sdd1 do not develop stomata, but the arrangement of the meristemoids is similar to the arrangement of the stomata induced by the mutation(s) in the signalling gene(s) in each case [4]. This suggests that all these genes interact additively [4]. In addition, the absence of stomata in the double or quadruple mutants suggests that MUTE might act downstream of these genes triggering GMC formation [4]. The absence of stomata in mutant combinations between fama and the mutants of the signalling genes ( fama sdd1, fama tmm, fama er erl1 erl2 and fama yda) [2] also places FAMA downstream of such genes with respect to the regulation of guard cell differentiation. Moreover, the arrangement of the GMCs or immature guard cells reflects the phenotype of mutations in the signalling components [2], which suggests that they interact additively with FAMA. In addition to the bHLH regulators of stomatal development, two other proteins belonging to the MYB family of transcription factors have been implicated in this process [12]. Both FOUR LIPS and MYB88 control the formation of the stoma from the GMC [12]. Some MYB proteins regulate transcription by physical interaction with bHLH proteins [13]. However, FOUR LIPS, MYB88 and FAMA do not contain the amino acid signatures defined as necessary for the interaction between MYB and bHLH proteins [6]. Certainly, although several techniques have been used, no interactions between FOUR LIPS or MYB88 and FAMA have been detected [2]. Moreover, neither protein is required for the transcriptional
Update
TRENDS in Plant Science
activation of the other [2]. Together, this suggests that FAMA and FLP/MYB88 control the GMC–guard cell transition independently. Stomatal density is regulated by environmental conditions [14]. Environmental factors that increase stomatal density might be working through the positive regulators (SPCH, MUTE and FAMA). By contrast, those that decrease the number of stomata might be working through the negative ones (SDD1, TMM, ER-family, YDA and the MAPK module). Concluding remarks These results bring us closer to an understanding of how a stomatal precursor knows how often to divide. Among the many challenges that lie ahead is deciphering how SPCH, MUTE and FAMA interact with one another. It would also be interesting to determine not only which genes are regulated by these bHLH proteins, but also how their products function to ensure that fully differentiated stomata develop in the right places. *Note added in proof A new paper covering the same topic has been published during the production of this issue: Pillitteri, L.J. and Torii, K.U (2007) Breaking the silence: three bHLH proteins direct cell-fate decisions during stomatal development. Bioessays 29, 861–870. Acknowledgements I thank C. Martin for critical reading of the manuscript. Work in my laboratory is supported by grants from both the Communities Council of
Vol.12 No.11
485
Castilla-La Mancha (PAI-05–058) and the Ministry of Education and Culture of Spain (BIO2005–04493).
References 1 Bergmann, D.C. and Sack, F.D. (2007) Stomatal Development. Annu. Rev. Plant Biol. 58, 163–181 2 Ohashi-Ito, K. and Bergmann, D.C. (2006) Arabidopsis FAMA controls the final proliferation/differentiation switch during stomatal development. Plant Cell 18, 2493–2505 3 MacAlister, C.A. et al. (2007) Transcription factor control of asymmetric cell divisions that establish the stomatal lineage. Nature 445, 537–540 4 Pillitteri, L.J. et al. (2007) Termination of asymmetric cell division and differentiation of stomata. Nature 445, 501–505 5 Gray, J.E. (2007) Plant development: three steps for stomata. Curr. Biol. 17, R213–R215 6 Barton, M.K. (2007) Making holes in leaves: promoting cell state transitions in stomatal development. Plant Cell 19, 1140–1143 7 Berger, D. and Altmann, T. (2002) A subtilisin-like protease involved in the regulation of stomatal density and distribution in Arabidopsis thaliana. Genes Dev. 14, 1119–1131 8 Nadeau, J.A. and Sack, F.D. (2002) Control of stomatal distribution on the Arabidopsis leaf surface. Science 296, 1697–1700 9 Shpak, E.D. et al. (2005) Stomatal patterning and differentiation by synergistic interactions of receptor kinases. Science 309, 290–293 10 Bergmann, D.C. et al. (2004) Stomatal development and pattern controlled by a MAPKK kinase. Science 304, 1494–1497 11 Wang, H. et al. (2007) Stomatal development and patterning are regulated by environmentally responsive mitogen-activated protein kinases in Arabidopsis. Plant Cell 19, 63–73 12 Lai, L.B. et al. (2005) The Arabidopsis R2R3 MYB proteins FOUR LIPS and MYB88 restrict divisions late in the stomatal lineage. Plant Cell 17, 2754–2767 13 Serna, L. and Martin, C. (2006) Trichomes: different regulatory networks lead to convergent structures. Trends Plant Sci. 11, 274–280 14 Hetherington, A.M. and Woodward, F.I. (2003) The role of stomata in sensing and driving environmental change. Nature 424, 901–908
Symposium Announcement Evolution of Weediness and Invasiveness: Molecular Genetics Approaches February 7, 2008. Hilton Chicago, 720 South Michigan Ave., Chicago, Illinois. A one day symposium and workshop on the use of molecular genomics in weed science will be held in conjunction with the 2008 annual meeting of the Weed Science Society of America, February 4-7, 2008 in Chicago (wssa.net). The symposium portion will feature speakers such as Steve Duke, Jonathan Gressel, Loren Rieseberg, and Rod Wing. Following the complimentary lunch, the workshop portion of the conference will conclude with breakout sessions to discuss and determine the path forward in applying tools from the genomics revolution to weed science. The symposium is organized by Pat Tranel and Neal Stewart. Registration is via the WSSA website (wssa.net). www.sciencedirect.com