Skip to main content
. 2004 Aug 15;18(16):1964–1969. doi: 10.1101/gad.305504

Figure 1.

Figure 1.

Site-specific SCR gene activation and deletion to investigate alternative possibilities for SCR function in asymmetric division. (a) Schematic representation of cell types present in the Arabidopsis root meristem. Radially organized are the stele (St), endodermis (En), cortex (Cor), epidermis (Epi), and lateral root cap (Lrc). In the proximal-distal plane, quiescent center (QC) and columella (Col). (gtsc) Ground tissue stem cell; (scd) stem cell daughter. (b) Possibilities for SCR function in establishing asymmetry during periclinal ground tissue cell division. SCR is required for the execution of the periclinal division (1,2,3). (1) SCR and SHR are required to maintain endodermis fate; C determines cortex fate. (2) SCR plays no part in division asymmetry, only external factors determine endodermal and cortex fate. (3) During periclinal division, SCR separates endodermis and cortex fates. (c) Two possible signaling pathways allowing periclinal cell division in the ground tissue stem cell daughters. (1) Mature cells act as a patterning template and reinforce periclinal cell division. (2) QC signaling prevents differentiation and periclinal division in the stem cell. (d) Clonal SCR gene activation in scr-4 using vectors pCB1 and pG7HSCRE-USCR. Heat-shock activation of CRE recombinase mediates excision of the sequences between the direct repeat lox recombination sites. The 35S constitutive promoter then drives GAL4VP16 expression, resulting in transactivation of SCR expression and GFPER, thereby marking the cells with recombination events. (e) Clonal deletion of SCR using pCB1-SCR complemented scr-4 and pG7HSCRE. Heat-shock activation of CRE recombinase mediates excision of SCR, resulting in the 35S-driven GAL4VP16 and transactivation of GFPER expression, thereby marking the scr-4 mutant cells. Color-filled objects represent active promoters (green), transcribed genes (blue, green, orange, yellow), and terminators (red).