![]() Cell divisions in the pericycle have given rise to a mound of tissue composed of small, densely cytoplasmic cells. (B) A longitudinal section of the parent root through the center of a lateral primordium at a later stage. An endodermis (E) is indicated by arrows. Arrowheads indicate the extent of pericycle tissue involved. Periclinal and anticlinal divisions in the pericycle (P) opposite a xylem pole (Xy) herald the development of a lateral primordium. (A) A transverse section of the parent root showing an early stage. Development of a lateral root in Zea mays. The direct targets of KRP2 remain to be explored in greater detail, and one would propose that direct down-regulation of KRP2 targets would result in decreased LRP initiation, while the over-expression of those targets would overcome the LRP reduction in the KRP2 over-expressing background.įIGURE 14-8. Therefore, a model has been proposed where: (1) KRP2 inhibits progression of xylem-pole pericycle cells through the cell cycle (2) down-regulation of KRP2 in specific cells within a certain developmental window allows those cells to continue through the cell cycle and (3) other cells retain high KRP2 expression and are not competent to progress through the cell cycle ( Casimiro et al., 2003 Himanen et al., 2002). Furthermore, over-expression of KRP2 resulted in the strong inhibition of LRP initiation. The down-regulation of these cell cycle inhibitors correlated with the progression of initiated pericycle cells through the cell cycle. These results were corroborated later in a more extensive microarray study ( Himanen et al., 2004). Intriguingly, it was found that the CDK inhibitors KRP1 and KRP2 were initially highly expressed in synchronised, initiating pericycle cells and subsequently down-regulated within 4 h of lateral root initiation ( Himanen et al., 2002). This result shows that CycB1 1 alone is not sufficient to drive LRP initiation. The CycB1 1 gene had been associated with LRP initiation previously ( Doerner et al., 1996) however, ectopic expression of CycB1 1 with the CDKA 1 promoter failed to increase the number of LRP. This is evidenced by later expression of the G2-M specific genes CycB1 1, CycB1 2, CDKB1 1 and CDKB2 2 in synchronised, initiating cells ( Himanen et al., 2002). Certain xylem-pole pericycle cells then become competent to progress through the G1–S transition and on to the G2-M checkpoint ( Casimiro et al., 2003). Interestingly, over-expression of CycD3 1 in the pericycle did not lead to an increased number of LRP, showing that it is not sufficient to promote LRP initiation ( de Jager et al., 2005). In addition, the G1–S-specific CDKA 1 is constitutively active in the xylem-pole pericycle cells ( Himanen et al., 2002). Consistent with this, the G1–S-specific CycD4 1 and CycD3 1 genes show expression associated with LRP initiation ( De Veylder et al., 1999 Himanen et al., 2002). A detailed transcriptome study of lateral root initiation using a synchronised population of pericycle cells that were simultaneously activated to form LRP showed that all pericycle cells are initially held at the G1–S checkpoint ( Himanen et al., 2002). LRP formation involves the controlled progression of anti- and periclinal cell divisions and specific cell cycle components have been identified in the regulation of this process ( de Jager et al., 2005 De Smet et al., 2006 Himanen et al., 2002 Malamy, 2005 Osmont et al., 2007). Malamy, in Advances in Botanical Research, 2010 2 Cell cycle control in the LRP ![]()
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