The phytohormone abscisic acid (ABA) plays an essential role in plant development and during the response of the plant to abiotic stress. In this study, we report that the R2R3-type transcription factor MYB30 is involved in the regulation of ABA signaling. Arabidopsis mutants lacking MYB30 are hypersensitive to ABA during germination and seedling growth. A K283R substitution in MYB30 blocks its SUMO E3 ligase SIZ1-mediated sumoylation in Arabidopsis protoplasts, indicating that MYB30 is sumoylated by SIZ1 and that K283 is the principal site for small ubiquitin-like modifier conjugation. Expression of MYB30 K283R in myb30 partially rescues the mutant ABA-hypersensitive phenotype, but expression of wild-type MYB30 complements the mutant phenotype. Overexpression of MYB30 in wild-type results in an ABA-insensitive phenotype, whereas overexpression of MYB30 in the siz1 mutant does not alter siz1 hypersensitivity to ABA. The siz1-2 myb30-2 double-mutant exhibits greater ABA sensitivity than either single mutant, but a mutation in the SIZ1-sumoylated ABI5 transcription factor suppresses the ABA hypersensitivity of myb30-2 to wild-type levels. Our results suggest that coordination of ABI5 and MYB30 sumoylation by SIZ1 may balance gene expression, which is required for regulation of ABA signaling during seed germination.A bscisic acid (ABA) plays important roles throughout the life cycle of the plant, including during seed development and dormancy, seed germination, early seedling development, flowering, and in response to abiotic and biotic stress. Genetic studies have revealed that a number of loci are essential for ABA biosynthesis (1-5), catabolism (6, 7), and signal transduction (8, 9) in plants.A number of studies have focused on understanding ABA signaling from perception to response. Recently, three groups of ABA receptors (ABAR/GUN5, GRGC/GTG, and PYR/PYL/ RCAR) have been identified in Arabidopsis and shown to bind ABA with high affinity (10-14). The various functions and cellular locations of these ABA receptors point to the complexity of ABA signaling. For example, PYR/PYL/RCAR-modulated ABA signaling has been studied extensively and found to involve a double-negative regulatory system that includes the receptor, protein phosphatases (PP2C), and protein kinases (SnRK2) (15, 16).A group of basic leucine zipper transcription factors, including ABI5, serve as the downstream targets of SnRK2 and phosphorylation is correlated with ABI5 transcriptional activity and protein stability (17-19). ABI5 undergoes 26S proteasome-mediated degradation and ABA stabilizes the ABI5 protein (17). Two ABI5 interacting proteins, AFP (ABI5-interacting protein) and KEG (KEEP ON GOING, a RING-finger ubiquitin E3 ligase) are required for ABI5 degradation (20,21). Arabidopsis lacking either gene is hypersensitive to ABA and an abi5 mutation suppresses the ABA sensitivity of both the afp-1 and keg mutants (20,21). Recently it has been shown that ABI5 is sumoylated by the small ubiquitin-like modifier (SUMO) E3 ligase SIZ1 at amino acid ...

Cytosolic calcium signaling is critical for regulating downstream responses in plants encountering unfavorable environmental conditions. In a genetic screen for Arabidopsis thaliana mutants defective in stress-induced cytosolic free Ca ([Ca ] ) elevations, we identified the R2R3-MYB transcription factor MYB30 as a regulator of [Ca ] in response to H O and heat stresses. Plants lacking MYB30 protein exhibited greater elevation of [Ca ] in response to oxidative and heat stimuli. Real-time reverse transcription-polymerase chain reaction (RT-PCR) results indicated that the expression of a number of ANNEXIN (ANN) genes, which encode Ca -regulated membrane-binding proteins modulating cytosolic calcium signatures, were upregulated in myb30 mutants. Further analysis showed that MYB30 bound to the promoters of ANN1 and ANN4 and repressed their expression. myb30 mutants were sensitive to methyl viologen (MV) and heat stresses. The H O - and heat-induced abnormal [Ca ] in myb30 was dependent on the function of ANN proteins. Moreover, the MV and heat sensitivity of myb30 was suppressed in mutants lacking ANN function or by application of LaCl , a calcium channel blocker. These results indicate that MYB30 regulates oxidative and heat stress responses through calcium signaling, which is at least partially mediated by ANN1 and ANN4.

Plants face a more volatile environment than other organisms because of their immobility, and they have developed highly efficient mechanisms to adapt to stress conditions. Transcription factors, as an important part of the adaptation process, are activated by different signals and are responsible for the expression of stress-responsive genes. MYB transcription factors, as one of the most widespread transcription factor families in plants, participate in plant development and responses to stresses by combining with MYB cis-elements in promoters of target genes. MYB transcription factors have been extensively studied and have proven to be critical in the biosynthesis of secondary metabolites in plants, including anthocyanins, flavonols, and lignin. Multiple studies have now shown that MYB proteins play diverse roles in the responses to abiotic stresses, such as drought, salt, and cold stresses. However, the regulatory mechanism of MYB proteins in abiotic stresses is still not well understood. In this review, we will focus mainly on the function of Arabidopsis MYB transcription factors in abiotic stresses, especially how MYB proteins participate in these stress responses. We also pay attention to how the MYB proteins are regulated in these processes at both the transcript and protein levels.

This study was designed to investigate the protective effect of curcumin against d-galactose (d-gal)-induced premature ovarian failure (POF) in mice. A mouse POF model was induced by subcutaneous injection of d-gal (200 mg/kg/day) daily for 42 days. Mice in the curcumin group received both d-gal treatment and intraperitoneal injection of curcumin (100 mg/kg/day) for 42 days. Ovarian function, oxidative stress and apoptosis were evaluated. The P, E2 and SOD levels were higher, and the FSH, LH and MDA levels were significantly lower in the curcumin group than those in the d-gal group. The proportion of primordial follicles was also significantly higher in the curcumin group than that in the d-gal group. In addition, curcumin treatment after d-gal administration resulted in significantly lower Sod2, Cat, 8-OhdG, 4-HNE, NTY and senescence-associated protein P16 expression levels, higher Amh expression levels and less apoptosis in granulosa cells than was observed in the d-gal group. Moreover, the p-Akt, Nrf2 and HO-1 protein expression levels were significantly higher and the apoptosis-related cleaved caspase-3 and -9 protein expression levels were markedly lower in the curcumin group than in the d-gal group. In conclusion, curcumin effectively inhibited d-gal-induced oxidative stress, apoptosis and ovarian injury via a mechanism involving the Nrf2/HO-1 and PI3K/Akt signaling pathways, suggesting that curcumin is a potential protective agent against POF.