Tiller angle, a key agronomic trait for achieving ideal plant architecture and increasing grain yield, is regulated mainly by shoot gravitropism. Strigolactones (SLs) are a group of newly identified plant hormones that are essential for shoot branching/rice tillering and have further biological functions as yet undetermined. Through screening for suppressors of lazy1 (sols), a classic rice mutant exhibiting large tiller angle and defective shoot gravitropism, we identified multiple SOLS that are involved in the SL biosynthetic or signaling pathway. We show that SL biosynthetic or signaling mutants can rescue the spreading phenotype of lazy1 (la1) and that SLs can inhibit auxin biosynthesis and attenuate rice shoot gravitropism, mainly by decreasing the local indoleacetic acid content. Although both SLs and LA1 are negative regulators of polar auxin transport, SLs do not alter the lateral auxin transport of shoot base, unlike LA1, which is a positive regulator of lateral auxin transport in rice. Genetic evidence demonstrates that SLs and LA1 participate in regulating shoot gravitropism and tiller angle in distinct genetic pathways. In addition, the SL-mediated shoot gravitropism is conserved in Arabidopsis. Our results disclose a new role of SLs and shed light on a previously unidentified mechanism underlying shoot gravitropism. Our study indicates that SLs could be considered as an important tool to achieve ideal plant architecture in the future.
Epithelial-mesenchymal transition (EMT) has been reported to play a significant role in tumour metastasis as well as chemoresistance. However, the molecular mechanisms involved in chemotherapy-induced EMT are still unclear. MicroRNA (miRNA) expression and functions have been reported to contribute to phenotypic features of tumour cells. To investigate the roles of miRNAs in chemotherapy-induced EMT, we established two docetaxel-resistant lung adenocarcinoma (LAD) cell models (SPC-A1/DTX and H1299/DTX), which display EMT-like properties and gain increased invasion or migration activity. MiR-451 was found to be significantly downregulated in docetaxel-resistant LAD cells, and re-expression of miR-451 could reverse EMT to mesenchymal-epithelial transition (MET) and inhibit invasion and metastasis of docetaxel-resistant LAD cells both in vitro and in vivo. The proto-oncogene c-Myc was identified as a direct and functional target of miR-451, and further researches confirmed that overexpression of c-Myc which induced extracellular-signal-regulated kinase (ERK)-dependent glycogen synthase kinase-3 beta (GSK-3?) inactivation and subsequent snail activation is essential for acquisition of EMT phenotype induced by loss of miR-451. Furthermore, c-Myc was significantly upregulated in docetaxel-non-responding LAD tissues in comparison with docetaxel-responding tissues, and its expression was inversely correlated with miR-451 expression. This study first reported the involvement of miR-451/c-Myc/ERK/GSK-3? signalling axis in the acquisition of EMT phenotype in docetaxel-resistant LAD cells, suggesting that re-expression of miR-451 or targeting c-Myc will be a potential strategy for the treatment of chemoresistant LAD patients.
Docetaxel resistance remains a major obstacle in the treatment of non-small cell lung cancer (NSCLC). High-mobility group box 1 (HMGB1) has been shown to promote autophagy protection in response to antitumor therapy, but the exact molecular mechanism underlying HMGB1-mediated autophagy has not been clearly defined.
The critical developmental switch from heterotrophic to autotrophic growth of plants involves light signaling transduction and the production of reactive oxygen species (ROS). ROS function as signaling molecules that regulate multiple developmental processes, including cell death. However, the relationship between light and ROS signaling remains unclear. Here, we identify transcriptional modules composed of the basic helix-loop-helix and bZIP transcription factors PHYTOCHROME-INTERACTING FACTOR1 (PIF1), PIF3, ELONGATED HYPOCOTYL5 (HY5), and HY5 HOMOLOGY (HYH) that bridge light and ROS signaling to regulate cell death and photooxidative response. We show that pif mutants release more singlet oxygen and exhibit more extensive cell death than the wild type during Arabidopsis thaliana deetiolation. Genome-wide expression profiling indicates that PIF1 represses numerous ROS and stress-related genes. Molecular and biochemical analyses reveal that PIF1/PIF3 and HY5/HYH physically interact and coordinately regulate the expression of five ROS-responsive genes by directly binding to their promoters. Furthermore, PIF1/PIF3 and HY5/HYH function antagonistically during the seedling greening process. In addition, phytochromes, cryptochromes, and CONSTITUTIVE PHOTOMORPHOGENIC1 act upstream to regulate ROS signaling. Together, this study reveals that the PIF1/PIF3-HY5/HYH transcriptional modules mediate crosstalk between light and ROS signaling and sheds light on a new mechanism by which plants adapt to the light environments.
Carotenoids with conjugated carbonyl groups possess special photophysical properties which have been studied in some water-soluble light-harvesting proteins (Polívka and Sundström, Chem Rev 104:2021-2071, 2004). However, siphonaxanthin-type light-harvesting complexes of photosystem II (LHCII) in siphonous green alga have received fewer studies. In the present study, we determined sequences of genes for several Bryopsis corticulans Lhcbm proteins, which showed that they belong to the group of major LHCII and diverged early from green algae and higher plants. Analysis of pigment composition indicated that this siphonaxanthin-type LHCII contained in total 3 siphonaxanthin and siphonein but no lutein and violaxanthin. In addition, 2 chlorophylls a in higher plant LHCII were replaced by chlorophyll b. These changes led to an increased absorption in green and blue-green light region compared with higher plant LHCII. The binding sites for chlorophylls, siphonaxanthin, and siphonein were suggested based on the structural comparison with that of higher plant LHCII. All of the ligands for the chlorophylls were completely conserved, suggesting that the two chlorophylls b were replaced by chlorophyll a without changing their binding sites in higher plant LHCII. Comparisons of the absorption spectra of isolated siphonaxanthin and siphonein in different organic solutions and the effect of heat treatment suggested that these pigments existed in a low hydrophobic protein environment, leading to an enhancement of light harvesting in the green light region. This low hydrophobic protein environment was maintained by the presence of more serine and threonine residues in B. corticulans LHCII. Finally, esterization of siphonein may also contribute to the enhanced harvesting of green light.
Photomorphogenesis is a critical plant developmental process that involves light-mediated transcriptome changes, histone modifications, and inhibition of hypocotyl growth. However, the chromatin-based regulatory mechanism underlying this process remains largely unknown. Here, we identify ENHANCED PHOTOMORPHOGENIC1 (EPP1), previously known as PICKLE (PKL), an ATP-dependent chromatin remodeling factor of the chromodomain/helicase/DNA binding family, as a repressor of photomorphogenesis in Arabidopsis thaliana. We show that PKL/EPP1 expression is repressed by light in the hypocotyls in a photoreceptor-dependent manner. Furthermore, we reveal that the transcription factor ELONGATED HYPOCOTYL5 (HY5) binds to the promoters of cell elongation-related genes and recruits PKL/EPP1 through their physical interaction. PKL/EPP1 in turn negatively regulates HY5 by repressing trimethylation of histone H3 Lys 27 at the target loci, thereby regulating the expression of these genes and, thus, hypocotyl elongation. We also show that HY5 possesses transcriptional repression activity. Our study reveals a crucial role for a chromatin remodeling factor in repressing photomorphogenesis and demonstrates that transcription factor-mediated recruitment of chromatin-remodeling machinery is important for plant development in response to changing light environments.
Successful chlorophyll biosynthesis during initial light exposure is critical for plant survival and growth, as excess accumulation of chlorophyll precursors in darkness can cause photooxidative damage to cells. Therefore, efficient mechanisms have evolved to precisely regulate chlorophyll biosynthesis in plants. Here, we identify FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and FAR-RED IMPAIRED RESPONSE1 (FAR1), two transposase-derived transcription factors, as positive regulators of chlorophyll biosynthesis in Arabidopsis thaliana. We show that null mutations in FHY3 and FAR1 cause reduced protochlorophyllide (a precursor of chlorophyll) levels in darkness and less photobleaching in the light. We find that FHY3 directly binds to the promoter and activates expression of HEMB1, which encodes 5-aminolevulinic acid dehydratase in the chlorophyll biosynthetic pathway. We reveal that PHYTOCHROME-INTERACTING FACTOR1 physically interacts with the DNA binding domain of FHY3, thereby partly repressing FHY3/FAR1-activated HEMB1 expression. Strikingly, FHY3 expression is upregulated by white light. In addition, our genetic data indicate that overexpression, severe reduction, or lack of HEMB1 impairs plant growth and development. Together, our findings reveal a crucial role of FHY3/FAR1 in regulating chlorophyll biosynthesis, thus uncovering a new layer of regulation by which light promotes plant dark-light transition in early seedling development.
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