Aba

enzymatic steps (Fig. 24.4). The salinity stress-induced activation of many ABA biosynthetic genes, such as zeaxanthin oxidase, 9-as-epoxycarotenoid dioxygenase, ABA-aldehyde oxidase, and molybdenum cofactor sulfurase, appear to be regulated through a calcium-dependent phosphorylation pathway (Fig. 24.4) (reviewed by Chinnusamy et al., 2004; Xiong et al., 2002; Zhu, 2002). The accumulation of ABA can also stimulate the expression of ABA biosynthetic genes through a calcium-signaling pathway and can also activate the ABA catabolic enzymes to degrade the ABA.

The induction of osmotic stress responsive genes imposed by salinity is transmitted through either ABA-dependent or ABA-independent pathways, although some others are only partially ABA dependent (Shinozaki et al., 1997). However, the components involved in these pathways often cross talk through calcium in stress signaling pathways.

The transcript accumulation of the RD29A gene is reported to be regulated in both ABA-dependent and ABA-independent manners (Yamaguchi-Shinozaki et al., 1993). The proline accumulation in plants can be mediated by both ABA-dependent and ABA-independent signaling pathways (see Zhu, 2002). The salinity stress-induced upregulation of the transcript of pea DNA helicase 45 (PDH45) followed the ABA-dependent pathway (Sanan-Mishra et al., 2005), whereas the CBL and CIPK from pea followed the ABA-independent pathway (Mahajan et al., 2006b). The role of calcium in ABA-dependent induction of the P5CS gene during salinity stress has been reported by Kinight et al. (1997). It is also suggested that phospholipase D, along with ABA and calcium, acts as a negative regulator of proline biosynthesis in Arabidopsis (Thiery et al., 2004). The signaling mechanism behind the activation of these genes is not well known, but the transcriptional activation of a few stress-induced genes represented by RD29A is known to some extent (see Xiong et al., 2002). It is known that the expression of RD29A, RD22, COR15A, COR47, and P5CS genes was reduced in the los5mutant (Xiong etal., 2001). Overall, the ABA-dependent pathways are involved essentially in osmotic stress gene expression.

The transcriptional regulatory network of cis-acting elements and transcription factors involved in ABA and salinity stress responsive gene expression is depicted in Fig. 24.5. Promoters of the stress-induced genes contain cis-regulatory elements such as DRE/CRT, ABRE, MYC recognition sequence (MYCRS), and MYB recognition sequence (MYBRS), which are regulated by various upstream transcriptional factors (Fig. 24.5) (see Mahajan et al., 2005; Zhu, 2002). The ABA-dependent salinity stress signaling activates basic leucine zipper transcription factors called AREB, which bind to ABRE element to induce the stress responsive gene (RD29A). Transcription factors such as DREB2A and DREB2B transacti-vate the DRE cis element of osmotic stress genes and thereby are involved in maintaining the osmotic equilibrium of the cell (see Mahajan and Tuteja, 2005). Some genes, such as RAD22, lack the typical CRT/DRE elements

DRE/CRT ABRE MYCRS

MYBRS mRNA

Figure 24.5 Transcriptional regulatory network of cis-acting elements and ABA-dependent transcription factors involved in salinity stress gene expression. Osmotic stress signaling generated via salinity stress seems to be mediated by transcription factors such as DREB2A/DREB2B, AREB1, and MYC/MYB transcription activators, which interact with DRE/CRT, ABRE, and MYCRS/MYBRS elements in the promotion of stress genes, respectively. AtMYC2 and AtMYB2 act cooperatively to activate the expression ofABA-inducible genes such as RD22. Transcription factor-binding sites are represented as rectangles at the bottom ofthe figure, with the representative promoters. Salinity works mainly through the SOS pathway, reinstating cellular ionic equilibrium.

DRE/CRT ABRE MYCRS

MYBRS mRNA

Figure 24.5 Transcriptional regulatory network of cis-acting elements and ABA-dependent transcription factors involved in salinity stress gene expression. Osmotic stress signaling generated via salinity stress seems to be mediated by transcription factors such as DREB2A/DREB2B, AREB1, and MYC/MYB transcription activators, which interact with DRE/CRT, ABRE, and MYCRS/MYBRS elements in the promotion of stress genes, respectively. AtMYC2 and AtMYB2 act cooperatively to activate the expression ofABA-inducible genes such as RD22. Transcription factor-binding sites are represented as rectangles at the bottom ofthe figure, with the representative promoters. Salinity works mainly through the SOS pathway, reinstating cellular ionic equilibrium.

in their promoter, suggesting their regulation by some other mechanism. The MYC/MYB transcription factors RD22BP1 and AtMYB2 could bind MYCRS and MYBRS elements, respectively, and help in activation of the RD22 gene (Fig. 24.5). Overall, these transcription factors may also cross talk with each other for their maximal response to stress tolerance.

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