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SUMMARY: Mediator 17 (MED17) is a subunit of the Mediator complex that regulates transcription initiation in eukaryotic organisms. In yeast and humans, MED17 also participates in DNA repair, physically interacting with proteins of the nucleotide excision DNA repair system, but this function in plants has not been investigated. We studied the role of MED17 in Arabidopsis plants exposed to UV‐B radiation. Our results demonstrate that med17 and OE MED17 plants have altered responses to UV‐B, and that MED17 participates in various aspects of the DNA damage response (DDR). Comparison of the med17 transcriptome with that of wild‐type (WT) plants showed that almost one‐third of transcripts with altered expression in med17 plants were also changed by UV‐B exposure in WT plants. Increased sensitivity to DNA damage after UV‐B in med17 plants could result from the altered regulation of UV‐B responsive transcripts but MED17 also physically interacts with DNA repair proteins, suggesting a direct role of this Mediator subunit during repair. Finally, we show that MED17 is necessary to regulate the DDR activated by ataxia telangiectasia and Rad3 related (ATR), and that programmed cell death 5 (PDCD5) overexpression reverts the deficiencies in DDR shown in med17 mutants. Our data demonstrate that MED17 is an important regulator of DDR after UV‐B irradiation in Arabidopsis. Significance Statement: In Arabidopsis, MED17 regulates the DNA damage response after UV‐B exposure transcriptionally modulating the expression of genes and possibly also physically interacting with DNA repair proteins. [ABSTRACT FROM AUTHOR]

SUMMARY: Ultraviolet (UV)B radiation affects plant growth inhibiting cell proliferation. This inhibition is in part controlled by the activity of transcription factors from the E2F family. In particular, the participation of E2Fc and E2Fe in UV‐B responses in Arabidopsis plants was previously reported. However, the E2Fa and E2Fb contribution to these processes has still not been investigated. Thus, in this work, we provide evidence that, in Arabidopsis, both E2Fa and E2Fb control leaf size under UV‐B conditions without participating in the repair of cyclobutane pyrimidine dimers in the DNA. Nevertheless, in UV‐B‐exposed seedlings, E2Fa, but not E2Fb, regulates primary root elongation, cell proliferation, and programmed cell death in the meristematic zone. Using e2fa mutants that overexpress E2Fb, we showed that the role of E2Fa in the roots could not be replaced by E2Fb. Finally, our results show that E2Fa and E2Fb differentially regulate the expression of genes that activate the DNA damage response and cell cycle progression, both under conditions without UV‐B and after exposure. Overall, we showed that both E2Fa and E2Fb have different and non‐redundant roles in developmental and DNA damage responses in Arabidopsis plants exposed to UV‐B. [ABSTRACT FROM AUTHOR]

Summary: UV‐B radiation inhibits plant growth, and this inhibition is, to a certain extent, regulated by miR396‐mediated repression of Growth Regulating Transcription factors (GRFs). Moreover, E2Fe transcription factor also modulates Arabidopsis leaf growth. Here, we provide evidence that, at UV‐B intensities that induce DNA damage, E2Fc participates in the inhibition of cell proliferation. We demonstrate that E2Fc‐deficient plants show a lower inhibition of leaf size under UV‐B conditions that damage DNA, decreased cell death after exposure and altered SOG1 and ATR expression. Interestingly, the previously reported participation of E2Fe in UV‐B responses, which is a transcriptional target of E2Fc, is independent and different from that described for E2Fc. Conversely, we here demonstrate that E2Fc has an epistatic role over the miR396 pathway under UV‐B conditions. Finally, we show that inhibition of cell proliferation by UV‐B is independent of the regulation of class II TCP transcription factors. Together, our results demonstrate that E2Fc is required for miR396 activity on cell proliferation under UV‐B, and that its role is independent of E2Fe, probably modulating DNA damage responses through the regulation of SOG1 and ATR transcript levels. Significance Statement: At intensities that can induce DNA damage in Arabidopsis plants, E2Fc‐deficient plants show a lower inhibition of leaf size and an altered DNA damage response. The inhibition of plant growth by UV‐B mediated by E2Fc occurs epistatically over the microRNA396 and independently of E2Fe. [ABSTRACT FROM AUTHOR]

Summary: Pattern recognition receptors (PRR) and nucleotide‐binding leucine‐rich repeat proteins (NLR) are major components of the plant immune system responsible for pathogen detection. To date, the transcriptional regulation of PRR/NLR genes is poorly understood. Some PRR/NLR genes are affected by epigenetic changes of neighboring transposable elements (TEs) (cis regulation). We analyzed whether these genes can also respond to changes in the epigenetic marks of distal pericentromeric TEs (trans regulation). We found that Arabidopsis tissues infected with Pseudomonas syringae pv. tomato (Pst) initially induced the expression of pericentromeric TEs, and then repressed it by RNA‐directed DNA methylation (RdDM). The latter response was accompanied by the accumulation of small RNAs (sRNAs) mapping to the TEs. Curiously these sRNAs also mapped to distal PRR/NLR genes, which were controlled by RdDM but remained induced in the infected tissues. Then, we used non‐infected mom1 (Morpheus' molecule 1) mutants that expressed pericentromeric TEs to test if they lose repression of PRR/NLR genes. mom1 plants activated several PRR/NLR genes that were unlinked to MOM1‐targeted TEs, and showed enhanced resistance to Pst. Remarkably, the increased defenses of mom1 were abolished when MOM1/RdDM‐mediated pericentromeric TEs silencing was re‐established. Therefore, common sRNAs could control PRR/NLR genes and distal pericentromeric TEs and preferentially silence TEs when they are activated. Significance Statement: This work provides evidence of a trans‐regulatory activity between pericentromeric transposable elements (TEs) and PRR/NLR genes by sRNAs homologous to both types of loci. After infection with P. syringae pv. tomato these sRNAs increase and silence the TEs but not the PRR/NLR genes. Similar alterations could also occur in mom1 mutants. [ABSTRACT FROM AUTHOR]

Flavonols are important compounds for conditional male fertility in maize ( Zea mays) and other crops, and they also contribute to protecting plants from UV-B radiation. However, little continues to be known on how maize and other grasses synthesize flavonols, and how flavonol biosynthesis is regulated. By homology with an Arabidopsis flavonol synthase ( AtFLS1), we cloned a maize gene encoding a protein ( ZmFLS1) capable of converting the dihydrokaempferol (DHK) and dihydroquercetin (DHQ) dihydroflavonols to the corresponding flavonols, kaempferol (K) and quercetin (Q). Moreover, ZmFLS1 partially complements the flavonol deficiency of the Arabidopsis fls1 mutant, and restores anthocyanin accumulation to normal levels. We demonstrate that ZmFLS1 is under the control of the anthocyanin (C1/PL1 + R/B) and 3-deoxy flavonoid (P1) transcriptional regulators. Indeed, using chromatin immunoprecipitation (ChIP) experiments, we establish that ZmFLS1 is an immediate direct target of the P1 and C1/R regulatory complexes, revealing similar control as for earlier steps in the maize flavonoid pathway. Highlighting the importance of flavonols in UV-B protection, we also show that ZmFLS1 is induced in maize seedlings by UV-B, and that this induction is in part mediated by the increased expression of the P1, B and PL1 regulators. Together, our results identify a key flavonoid biosynthetic enzyme so far missed in maize and other monocots, and illustrate mechanisms by which flavonol accumulation is controlled in maize. [ABSTRACT FROM AUTHOR]

A comparative analysis, by expression profiling of maize, was performed to identify novel components in the mechanisms of maize responses to UV-B. Five high-altitude landraces grown from 2000 to 3400 m naturally receive higher UV-B fluence than plants at lower altitudes and similar latitudes. These high-altitude landraces were compared directly with a low-altitude line and with literature reports for other temperate maize lines. A microarray analysis demonstrated that among the UV-B responsive transcripts, several types of gene implicated in chromatin remodeling are differentially expressed before and after UV-B treatment in high-altitude lines. RNAi transgenic plants with lower expression of four such chromatin-associated genes exhibited hypersensitivity to UV-B by measurements of leaf arching, increased leaf chlorosis and necrosis, and altered UV-B regulation of selected genes. These results collectively suggest that genes involved in chromatin remodeling are crucial for UV-B acclimation and that some high-altitude lines exhibit adaptations to this challenge. [ABSTRACT FROM AUTHOR]