Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 14 February 2006
Vol. 2006, Issue 322, p. tw58
[DOI: 10.1126/stke.3222006tw58]

EDITORS' CHOICE

STEM CELLS Maintaining the Shoot Meristem Stem Cell Population

Stem cells in plant shoot meristems give rise to stems, leaves, and flowers. One arm of the meristem stem cell maintenance pathway involves a negative feedback loop between the stem cells and the cells of the organizing center (OC) beneath the stem cells. WUSHCEL (WUS), a transcription factor present in the OC, is essential for maintenance of the stem cells, and CLAVATA3 (CLV3), which is a peptide ligand produced by the stem cells, feeds back on the OC to inhibit WUS transcription. Thus, CLV3 promotes stem cell differentiation and WUS promotes stem cell maintenance. Two reports investigate meristem stem cell signaling.

Würschum et al. identified a dominant-negative mutation in the gene encoding APETALA2 (AP2) in a screen for mutations that inhibited shoot meristem development in Arabidopsis. The mutation was mapped to the first of two AP2 domains in the protein, and the plants were called l28 mutants. When l28 plants with the dominant-negative mutation in AP2 were crossed with plants with null mutations in the gene encoding AP2, the frequency of premature shoot meristem termination was increased. l28 plants also exhibited reduced expression of WUS and CLV3. Genetic crosses indicated that termination of the shoot meristem in the l28 plants required functional CLV3, because CLV3 loss of function rescued shoot meristem development. Analysis of l28 plants crossed with wus-null plants indicated that WUS and AP2 were in the same pathway controlling shoot meristem maintenance. Because l28 mutants did not exhibit an increase in CLV3 expression, the authors propose a model in which AP2 inhibits CLV3 signaling downstream of CLV3 transcription.

Ni and Clark suggest that CLV3 may be cleaved extracellularly to release the CLE domain, which is the active ligand. The Arabidopsis genome encodes several proteins with a CLE domain. Nine of thirteen intronless CLE genes rescued or partially rescued the phenotype of supernumerary flower organs in clv3-1 transgenic plants. Replacement of the CLE domain of the inactive CLE8 with the CLE domain of CLV3 resulted in complete rescue. Furthermore, replacement of all but the CLE domain of CLV3 with sequences of unrelated protein ERECTA also rescued the clv3-1 phenotype, suggesting that the CLE domain is the essential portion. When glutathione S-transferase (GST)-tagged CLV3 or CLE1, which was one of the CLE proteins that fully rescued the clv3-1 phenotype, was incubated with cauliflower protein extracts, proteolytic processing that released the CLE domain was observed. The CLE domain of CLV3 had been previously shown to alter root development, thus suggesting that this portion of the molecule may be the active region. Thus, the authors propose that CLV3 may be cleaved to release the active CLE peptide. However, it remains to be determined if CLV3 or the related CLE proteins encoded by the other members of the CLE gene family are cleaved in vivo and whether this cleavage is mediated by a specific protease involved in CLV3 signaling.

T. Würschum, R. Groβ-Hardt, T. Laux, APETALA2 regulates the stem cell niche in the Arabidopsis shoot meristem. Plant Cell 18, 295-307 (2006). [Abstract] [Full Text]

J. Ni, S. E. Clark, Evidence for functional conservation, sufficiency, and proteolytic processing of the CLAVATA3 CLE domain. Plant. Physiol. 140, 726-733 (2006). [Abstract] [Full Text]

Citation: Maintaining the Shoot Meristem Stem Cell Population. Sci. STKE 2006, tw58 (2006).



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882