SAD2, an Importin β-Like Protein, Is Required for UV-B Response in <i>Arabidopsis</i> by Mediating MYB4 Nuclear Trafficking

Zhao, Jinfeng; Zhang, Wenhui; Zhao, Yanping; Gong, Xun; Guo, Liu; Zhu, Guoli; Wang, Xuechen; Gong, Zhizhong; Schumaker, Karen S.; Guo, Yan

doi:10.1105/tpc.106.048900

Cited by 163 publications

(162 citation statements)

References 40 publications

(63 reference statements)

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“…Although URM9 is ubiquitously expressed and has pleiotropic functions (Verslues et al, 2006;Zhao et al, 2007), the only known cargo of URM9 to date is MYB4, the loss of which does not induce any morphological defects (Jin et al, 2000). urm9 did not disrupt the nuclear import of GL3-2xGFP, suggesting that URM9 does not ferry GL3 as a cargo, but affects GL3 subnuclear distribution in an indirect manner.…”

Section: The Role Of Nucleocytoplasmic Transport In Trichome Patterningmentioning

confidence: 99%

Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning inArabidopsis

et al. 2009

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Once attacked by herbivores, plants regenerate new leaves with increased trichome density as an inducible defense. Trichomes are specified from neighboring epidermal cells through local cell-cell interactions in the leaf primordia. However, the molecular mechanism of how herbivore-induced damage at older leaves remodels the pattern of trichome fate specification at newly forming leaves is largely unknown. In this study, we show that mutations in either the biosynthetic or signaling pathway of jasmonates (JAs), long-distance wound signals, abolish the wound-induced formation of trichomes. To identify the factors linking JA signaling to trichome fate specification, we isolated a novel class of mutants, unarmed (urm), which lack trichome induction but show otherwise normal responses to JAs. URM9 encodes an Importin β family protein, and URM23 is identical to TRANSPARENT TESTA GLABRA1 (TTG1), the product of which interacts with the bHLH transcription factor GLABRA3 (GL3). Loss of either URM9 or URM23 disrupts the subnuclear localization of GL3, thus implicating GL3 in trichome induction. The expression of GL3 was enhanced by JA treatment prior to trichome initiation. Genetic analysis of multiple trichome mutants shows that GL3, in concert with the R2R3-Myb transcription factor GLABRA1 (GL1), promotes trichome fate in response to JA in a dosage-dependent manner. These results indicate that GL3 is a key transcription factor of wound-induced trichome formation acting downstream of JA signaling in Arabidopsis.

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Section: The Role Of Nucleocytoplasmic Transport In Trichome Patterningmentioning

confidence: 99%

Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning inArabidopsis

et al. 2009

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“…The N. benthamiana leaves were used for infiltration as described previously (47). Total protein was extracted and the Co-IP was performed as described (48). A total of 10 g of 14-d-old seedlings for each genotype was used in the pull-down.…”

Section: Methodsmentioning

confidence: 99%

Physical coupling of activation and derepression activities to maintain an active transcriptional state at FLC

Yang

Howard

Dean

2016

Proc. Natl. Acad. Sci. U.S.A.

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Establishment and maintenance of gene expression states is central to development and differentiation. Transcriptional and epigenetic mechanisms interconnect in poorly understood ways to determine these states. We explore these mechanisms through dissection of the regulation of Arabidopsis thaliana FLOWERING LOCUS C (FLC). FLC can be present in a transcriptionally active state marked by H3K36me3 or a silent state marked by H3K27me3. Here, we investigate the trans factors modifying these opposing histone states and find a physical coupling in vivo between the H3K36 methyltransferase, SDG8, and the H3K27me3 demethylase, ELF6. Previous modeling has predicted this coupling would exist as it facilitates bistability of opposing histone states. We also find association of SDG8 with the transcription machinery, namely RNA polymerase II and the PAF1 complex. Delivery of the active histone modifications is therefore likely to be through transcription at the locus. SDG8 and ELF6 were found to influence the localization of each other on FLC chromatin, showing the functional importance of the interaction. In addition, both influenced accumulation of the associated H3K27me3 and H3K36me3 histone modifications at FLC. We propose the physical coupling of activation and derepression activities coordinates transcriptional activity and prevents ectopic silencing.epigenetic regulation | histone modifications | histone methyltransferase | histone demethylase | FLOWERING LOCUS C C hromatin-based transcriptional activity is particularly important in multicellular organisms, where cells differentiate into very different developmental states. Transcriptional states are induced by internal developmental signals or triggered by environmental conditions and are then epigenetically maintained through many cell divisions. Considerable evidence suggests that opposing histone modifications mark different transcriptional states (1-6). However, there is still great debate as to how histone-based transcriptional states are initially established and maintained through development (7,8). We used Arabidopsis FLOWERING LOCUS C (FLC) as a model gene to explore histone-based transcriptional regulation and epigenetic memory. Local chromatin states are critical for quantitatively controlling FLC expression (9). Active FLC expression requires functional FRIGIDA (FRI) and a set of histone modifying Trithorax homologs, Complex Proteins Associated with Set1 (COMPASS), RNA polymerase II Associated Factor 1 complex (PAF1C), and SET DOMAIN GROUP 8 (SDG8), the major H3K36 methyltransferase (10-17). Repression of FLC requires either the autonomous pathway, which coordinately influences transcriptional initiation and elongation with associated chromatin modulation, or vernalization, the cold-induced Polycomb silencing (18-21). Both of these involve accumulation of high levels of H3K27me3 at FLC (20-22). A series of FLC antisense transcripts (COOLAIR) contribute to these repression pathways (18,(23)(24)(25)(26) Opposing H3K36me3 and H3K27me3 states are particularly ...

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“…CPDs were determined by ELISA using an anti-TDM-2 antibody (Tanaka et al, 2002) according to the manufacturer's instructions. The ELISA assay procedure was performed as previously described (Zhao et al, 2007).…”

Section: Elisa Assaysmentioning

confidence: 99%

“…The constructs were introduced into A. tumefaciens strain GV3101 and transformed into wildtype Arabidopsis plants. GUS staining of the T2 transgenic lines was performed as described (Zhao et al, 2007).…”

Section: Gus Stainingmentioning

confidence: 99%

“…High doses of UV-B irradiation reduce plant growth and development by inducing structural damage to DNA and membranes and disrupting processes including photosynthesis, secondary metabolism, responses to stress, and photomorphogenesis (Frohnmeyer and Staiger, 2003). To prevent damage from UV irradiation, plants have developed various mechanisms, including increased accumulation of UV-absorbing pigments (flavonoids and hydroxycinnamic acid derivatives) (Li et al, 1993;Landry et al, 1995;Jin et al, 2000;Bieza and Lois, 2001;Kliebenstein et al, 2002;Oravecz et al, 2006;Zhao et al, 2007;Bashandy et al, 2009), activation of reactive oxygen species (Mackerness et al, 2001;Gao et al, 2008), and generation of DNA damage repair systems (Gallego et al, 2000;Liu et al, 2000Liu et al, , 2003Ulm et al, 2001;Sakamoto et al, 2003;Liang et al, 2006;Vonarx et al, 2006;Wang and Liu, 2006;Hidema et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Arabidopsis Cockayne Syndrome A-Like Proteins 1A and 1B Form a Complex with CULLIN4 and Damage DNA Binding Protein 1A and Regulate the Response to UV Irradiation

et al. 2010

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In plants, as in animals, DNA is constantly subject to chemical modification. UV-B irradiation is a major genotoxic agent and has significant effects on plant growth and development. Through forward genetic screening, we identified a UV-Bsensitive mutant (csaat1a-3) in Arabidopsis thaliana, in which expression of CSAat1A, encoding a Cockayne Syndrome A-like protein, is reduced due to insertion of a T-DNA in the promoter region. Arabidopsis lacking CSAat1A or its homolog CSAat1B is more sensitive to UV-B and the genotoxic drug methyl methanesulfonate and exhibits reduced transcriptioncoupled repair activity. Yeast two-hybrid analysis indicated that both CSAat1A and B interact with DDB1A (UV-Damage DNA Binding Protein1). Coimmunoprecipitation assays demonstrated that CSAat1A and B associate with the CULLIN4 (CUL4)-DDB1A complex in Arabidopsis. A split-yellow fluorescent protein assay showed that this interaction occurs in the nucleus, consistent with the idea that the CUL4-DDB1A-CSA complex functions as a nuclear E3 ubiquitin ligase. CSAat1A and B formed heterotetramers in Arabidopsis. Taken together, our data suggest that the plant CUL4-DDB1A CSAat1A and B complex represents a unique mechanism to promote ubiquitination of substrates in response to DNA damage.

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SAD2, an Importin β-Like Protein, Is Required for UV-B Response in Arabidopsis by Mediating MYB4 Nuclear Trafficking

Cited by 163 publications

References 40 publications

Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning inArabidopsis

Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning inArabidopsis

Physical coupling of activation and derepression activities to maintain an active transcriptional state at FLC

Arabidopsis Cockayne Syndrome A-Like Proteins 1A and 1B Form a Complex with CULLIN4 and Damage DNA Binding Protein 1A and Regulate the Response to UV Irradiation

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