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High temperatures causing heat stress disturb cellular homeostasis and impede growth and development in plants. Extensive agricultural losses are attributed to heat stress, often in combination with other stresses. Plants have evolved a variety of responses to heat stress to minimize damage and to protect themselves from further stress. A narrow temperature window separates growth from heat stress, and the range of temperatures conferring optimal growth often overlap with those producing heat stress. Heat stress induces a cytoplasmic heat stress response (HSR) in which heat shock transcription factors (HSFs) activate a constellation of genes encoding heat shock proteins (HSPs). Heat stress also induces the endoplasmic reticulum (ER)-localized unfolded protein response (UPR), which activates transcription factors that upregulate a different family of stress response genes. Heat stress also activates hormone responses and alternative RNA splicing, all of which may contribute to thermotolerance. Heat stress is often studied by subjecting plants to step increases in temperatures; however, more recent studies have demonstrated that heat shock responses occur under simulated field conditions in which temperatures are slowly ramped up to more moderate temperatures. Heat stress responses, assessed at a molecular level, could be used as traits for plant breeders to select for thermotolerance.

The majority of breast cancers are primarily hormone‐sensitive and can be managed by endocrine therapy, although therapy‐resistant or hormone‐refractory cancers need alternative treatments. Recently, increasing attention is being paid to RNA‐binding proteins (RBP) in cancer pathophysiology. The precise role of RBP in breast cancer, however, remains to be clarified. We herein show that an RBP non‐POU domain‐containing octamer binding (NONO) plays a critical role in the pathophysiology of breast cancers regardless of their hormone dependency. Clinicopathological and immunohistochemical study of 127 breast cancer cases showed that NONO is a significant independent prognostic factor for breast cancer patients. Notably, siRNA‐mediated NONO knockdown substantially repressed the proliferation of both hormone‐sensitive MCF‐7 and hormone‐refractory MB‐MDA‐231 breast cancer cells. Integrative analysis combined with expression microarray and RIP‐sequencing (RNA immunoprecipitation‐sequencing) showed that NONO post‐transcriptionally regulates the expression of cell proliferation‐related genes by binding to their mRNAs, as exemplified by S‐phase‐associated kinase 2 and E2F transcription factor 8. Overall, these results suggest that NONO is a key regulator for breast cancer proliferation through the pre‐mRNA splicing of cell proliferation‐related genes and could be a potential new diagnostic and therapeutic target for advanced disease. The present study shows that Drosophila behavior human splicing family RNA‐binding protein NONO plays a critical role in breast cancer tumorigenesis. Clinicopathological study defines that NONO immunoreactivity significantly correlates with poor overall and distant disease‐free survival of breast cancer patients. Cell‐based experiments show that NONO contributes to breast cancer proliferation by regulating SKP2 and E2F8 expression at the post‐transcriptional level. Our findings provide a new cancer strategy by applying NONO as a potential diagnostic and therapeutic target for breast cancer.

In the poultry industry, excessive fat deposition is considered an undesirable factor, affecting feed efficiency, meat production cost, meat quality, and consumer’s health. Efforts to reduce fat deposition in economically important animals, such as chicken, can be made through different strategies; including genetic selection, feeding strategies, housing, and environmental strategies, as well as hormone supplementation. Recent investigations at the molecular level have revealed the significant role of the transcriptional and post-transcriptional regulatory networks and their interaction on modulating fat metabolism in chickens. At the transcriptional level, different transcription factors are known to regulate the expression of lipogenic and adipogenic genes through various signaling pathways, affecting chicken fat metabolism. Alternatively, at the post-transcriptional level, the regulatory mechanism of microRNAs (miRNAs) on lipid metabolism and deposition has added a promising dimension to understand the structural and functional regulatory mechanism of lipid metabolism in chicken. Therefore, this review focuses on the progress made in unraveling the molecular function of genes, transcription factors, and more notably significant miRNAs responsible for regulating adipogenesis, lipogenesis, and fat deposition in chicken. Moreover, a better understanding of the molecular regulation of lipid metabolism will give researchers novel insights to use functional molecular markers, such as miRNAs, for selection against excessive fat deposition to improve chicken production efficiency and meat quality.

• Alternative splicing (AS) is emerging as a critical co-transcriptional regulation for plants in response to environmental stresses. Although multiple splicing factors have been linked to the salt-sensitive signaling network, the molecular mechanism remains unclear. • We discovered that a conserved serine/arginine-rich (SR)-like protein, SR45a, as a component of the spliceosome, was involved in post-transcriptional regulation of salinity tolerance in Arabidopsis thaliana. Furthermore, SR45a was required for the AS and messenger RNA (mRNA) maturation of several salt-tolerance genes. Two alternatively spliced variants of SR45a were induced by salt stress, full-length SR45a-1a and the truncated isoform SR45a-1b, respectively. Lines with overexpression of SR45a-1a and SR45a-1b exhibited hypersensitive to salt stress. • Our data indicated that SR45a directly interacted with the cap-binding complex (CBC) subunit cap-binding protein 20 (CBP20) which mediated salt-stress responses. Instead of binding to other spliceosome components, SR45a-1b promoted the association of SR45a-1a with CBP20, therefore mediating salt-stress signal transduction pathways. Additionally, the mutations in SR45a and CBP20 led to different salt-stress phenotypes. • Together, these results provide the evidence that SR45a-CBP20 acts as a regulatory complex to regulate the plant response to salt stress, through a regulatory mechanism to fine-tune the splicing factors, especially in stressful conditions.

Long non‐coding RNAs (lncRNAs), as part of the family of non‐protein‐coding transcripts, are implicated in the occurrence and progression of several cardiovascular diseases (CVDs). With recent advances in lncRNA research, these molecules are purported to regulate gene expression at multiple levels, thereby producing beneficial or detrimental biological effects during CVD pathogenesis. At the transcriptional level, lncRNAs affect gene expression by interacting with DNA and proteins, for example, components of chromatin‐modifying complexes, or transcription factors affecting chromatin status. These potential mechanisms suggest that lncRNAs guide proteins to specific gene loci (eg promoter regions), or forestall proteins to specific genomic sites via DNA binding. Additionally, some lncRNAs are required for correct chromatin conformation, which occurs via chromatin looping in enhancer‐like models. At the post‐transcriptional level, lncRNAs interact with RNA molecules, mainly microRNAs (miRNAs) and mRNAs, potentially regulating CVD pathophysiological processes. Moreover, lncRNAs appear to post‐transcriptionally modulate gene expression by participating in mRNA splicing, stability, degradation and translation. Thus, the purpose of this review is to provide a comprehensive summary of lncRNAs implicated in CVD biological processes, with an emphasis on potential mechanisms of action.

Maintenance of the tightly regulated homeostatic environment of the brain is facilitated by the blood–brain barrier (BBB). P-glycoprotein (P-gp), an ATP-binding cassette transporter, is expressed on the luminal surface of the endothelial cells in the BBB, and actively exports a wide variety of substrates to limit exposure of the vulnerable brain environment to waste buildup and neurotoxic compounds. Downregulation of P-gp expression and activity at the BBB have been reported with ageing and in neurodegenerative diseases. Upregulation of P-gp at the BBB contributes to poor therapeutic outcomes due to altered pharmacokinetics of CNS-acting drugs. The regulation of P-gp is highly complex, but unravelling the mechanisms involved may help the development of novel and nuanced strategies to modulate P-gp expression for therapeutic benefit. This review summarises the current understanding of P-gp regulation in the brain, encompassing the transcriptional, post-transcriptional and post-translational mechanisms that have been identified to affect P-gp expression and transport activity.

• MicroRNAs play important roles in the regulation of gene expression in plants and animals. However, little information is known about the action mechanism and function of fungal microRNA-like RNAs (milRNAs). • In this study, combining deep sequencing, molecular and histological assays, milRNAs and their targets in the phytopathogenic fungus Valsa mali were isolated and identified. A critical milRNA, Vm-milR16, was identified to adaptively regulate the expression of virulence genes. • Fourteen isolated milRNAs showed high expression abundance. Based on the assessment of a pathogenicity function of these milRNAs, Vm-milR16 was found to be a critical milRNA in V. mali by regulating sucrose non-fermenting 1 (VmSNF1), 4,5-DOPA dioxygenase extradiol (VmDODA), and a hypothetical protein (VmHy1). During V. mali infection, Vm-milR16 is downregulated, while its targets are upregulated. Overexpression of Vm-milR16, but not mutated Vm-milR16, significantly reduces the expression of targets and virulence of V. mali. Furthermore, deletion of VmSNF1, VmDODA and VmHy1 significantly reduce virulence of V. mali. All three targets seem to be essential for oxidative stress response and VmSNF1 is required for expression of pectinase genes during V. mali–host interaction. • Our results demonstrate Vm-milRNAs contributing to the infection of V. mali on apple trees by adaptively regulating virulence genes.

•  miR‐21 expression in cancer and other diseases •  Mechanisms of miR‐21 elevation in cancer: multi‐level regulatory control •  Transcriptional control •  Post‐trancriptional regulation •  miR‐21 functions in cancer •  Identification of direct miR‐21 targets •  miR‐21 in gliomas: targeting cell cycle, apoptosis and invasion •  miR‐21 networking and feedback regulation •  miR‐21 as a diagnostic and prognostic marker •  Potential therapeutic target •  Acknowledgements More than 1000 microRNAs (miRNAs) are expressed in human cells, some tissue or cell type specific, others considered as house‐keeping molecules. Functions and direct mRNA targets for some miRNAs have been relatively well studied over the last years. Every miRNA potentially regulates the expression of numerous protein‐coding genes (tens to hundreds), but it has become increasingly clear that not all miRNAs are equally important; diverse high‐throughput screenings of various systems have identified a limited number of key functional miRNAs over and over again. Particular miRNAs emerge as principal regulators that control major cell functions in various physiological and pathophysiological settings. Since its identification 3 years ago as the miRNA most commonly and strongly up‐regulated in human brain tumour glioblastoma [1], miR‐21 has attracted the attention of researchers in various fields, such as development, oncology, stem cell biology and aging, becoming one of the most studied miRNAs, along with let‐7, miR‐17–92 cluster (‘oncomir‐1’), miR‐155 and a few others. However, an miR‐21 knockout mouse has not yet been generated, and the data about miR‐21 functions in normal cells are still very limited. In this review, we summarise the current knowledge of miR‐21 functions in human disease, with an emphasis on its regulation, oncogenic role, targets in human cancers, potential as a disease biomarker and novel therapeutic target in oncology.

It has been reported that lipid biosynthesis in plant host root cells plays critical roles in legume‐fungal or ‐rhizobial symbioses, but little is known about its regulatory mechanism in legume–rhizobia interaction. Soybean WRINKLED1 (WRI1) a and b, with their alternative splicing (AS) products a’ and b’, are highly expressed in developing seeds and nodules, but their functions in soybean nodulation are not known. GmWRI1a and b differently promoted triacylglycerol (TAG) accumulation in both Arabidopsis wild‐type and wri1 mutant seeds and when they ectopically expressed in the soybean hairy roots. Transcriptome analysis revealed that 15 genes containing AW boxes in their promoters were targeted by GmWRI1s, including genes involved in glycolysis, fatty acid (FA) and TAG biosynthesis. GmWRI1a, GmWRI1b and b’ differentially transactivated most targeted genes. Overexpression of GmWRI1s affected phospholipid and galactolipid synthesis, soluble sugar and starch contents and led to increased nodule numbers, whereas GmWRI1 knockdown hairy roots interfered root glycolysis and lipid biosynthesis and resulted in fewer nodules. These phenomena in GmWRI1 mutants coincided with the altered expression of nodulation genes. Thus, GmWRI1‐regulated starch degradation, glycolysis and lipid biosynthesis were critical for nodulation. GmWRI1 mutants also altered auxin and other hormone‐related biosynthesis and hormone‐related genes, by which GmWRI1s may affect nodule development. The study expands the views for pleiotropic effects of WRI1s in regulating soybean seed filling and root nodulation.

Lignin is a heterogeneous polymer of aromatic subunits derived from phenylalanine. It is polymerized in intimate proximity to the polysaccharide components in plant cell walls and provides additional rigidity and compressive strength for plants. Understanding the regulatory mechanisms of lignin biosynthesis is important for genetic modification of the plant cell wall for agricultural and industrial applications. Over the past 10 years the transcriptional regulatory model of lignin biosynthesis has been established in plants. However, the role of post-transcriptional regulation is still largely unknown. Increasing evidence suggests that lignin biosynthesis pathway genes are also regulated by alternative splicing, microRNA, and long non-coding RNA. In this review, we briefly summarize recent progress on the transcriptional regulation, then we focus on reviewing progress on the post-transcriptional regulation of lignin biosynthesis pathway genes in the woody model plant Populus .