DNA methylation is a key epigenetic mark when occurring in the promoter and enhancer regions regulates the accessibility of the binding protein and gene transcription. DNA methylation is inheritable and can be de novo-synthesized, erased and reinstated, making it arguably one of the most dynamic upstream regulators for gene expression and the most influential pacer for development. Recent progress has demonstrated that two forms of cytosine methylation and two pathways for demethylation constitute ample complexity for an instructional program for orchestrated gene expression and development. The forum of the current discussion and review are whether there is such a program, if so what the DNA methylation program entails, and what environment can change the DNA methylation program. The translational implication of the DNA methylation program is also proposed.

The success of many enteric bacteria is hinged on the ability to tolerate environmental stress such as extreme acidity. The acid stress response (ASR) has been investigated in many enteric bacteria and has been shown to involve variable expression of a broad spectrum of genes involved in transcriptional regulation, metabolism, colonization and virulence; representing a linkage between acid tolerance and pathogenicity. Though the majority of ASR studies have been conducted in laboratory conditions and from the perspective of pathogenicity, the role of environmental reservoirs on acid adaptation has recently emerged as an important aspect of pathogenic microbial ecology. This mini-review profiles ASR in three opportunistic enteric pathogens and synthesizes recent work pertaining to the study of this dynamic response.

Chronic obstructive pulmonary disease (COPD) is a highly relevant disorder that induces respiratory muscle dysfunction. One prevalent symptom of COPD is resistive breathing which causes respiratory muscle to significantly increase the magnitude of contractions, resulting in reactive oxygen species (ROS) formation and oxidative stress. Through cellular signaling cascades, ROS activate molecules such as mitogen-activated protein kinases and nuclear factor-κB. These signaling molecules stimulate the release of cytokines which in turn cause damage to the diaphragm, involving sarcomeric disruptions. In response to COPD induced fatigue, the diaphragm undergoes a beneficial fiber-type shift to type I muscle fibers, which are more resistant to hypoxia than type II fibers. The lung hyperinflation that occurs in COPD also causes intercostal muscle dysfunction, thereby exacerbating COPD symptoms. In addition, COPD is known to have a connection with heart failure, diabetes, and aging, further decreasing respiratory function. Currently, there is no cure for this disorder. Nevertheless, various potential therapeutic strategies focusing on respiratory muscle have been identified including respiratory muscle training, β₂-agonist therapy, and lung volume reduction surgery. In this review, we will outline the role of COPD, oxidative stress, and related complications in respiratory muscle dysfunction.

The phospholipase A₂ (PLA₂) family members are critical regulators of membrane structure and lipid composition and have been implicated in neuroinflammation, oxidative stress and neurodegeneration. Here, we review the published data describing regulation of cPLA₂ and iPLA₂ gene expression. Based on promoter sequence, cPLA₂ expression can be regulated by glucocorticoid and pro-inflammatory cytokines, whereas transcription of iPLA₂ can be controlled in response to sterol level. RNA degradation in 3′ UTR and epigenetic mechanisms may be involved in the regulation of cPLA₂ and iPLA₂ expression, respectively. MicroRNA target sequences lie within cPLA₂ and iPLA₂ mRNAs. Together, these findings indicate differential regulation of cPLA₂ and iPLA₂ expression. It is hoped that determination of diverse regulatory mechanisms of the PLA₂ family may open new doors for development of novel therapeutic compounds that modulate PLA₂ expression and function in the treatment of brain diseases.

The Murphy Roths Large (MRL/MpJ) mice provide unique insights into wound repair and regeneration. These mice and the closely related MRL/MpJ-Fas^lpr/J and Large strains heal wounds made in multiple tissues without production of a fibrotic scar. The precise mechanism of this remarkable ability still eludes researchers, but some data has been generated and insights are being revealed. For example, MRL cells reepithelialize over dermal wound sites faster than cells of other mouse strains. This allows a blastema to develop beneath the protective layer. The MRL mice also have an altered basal immune system and an altered immune response to injury. In addition, MRL mice have differences in their tissue resident progenitor cells and certain cell cycle regulatory proteins. The difficulty often lies in separating the causative differences from the corollary differences. Remarkably, not every tissue in these mice heals scarlessly, and the specific type of wound and priming affect regeneration ability as well. The MRL/MpJ, MRL/MpJ-Fas^lpr/J, and Large mouse strains are also being investigated for their autoimmune characteristic. Whether the two phenotypes of regeneration and autoimmunity are related remains an enigma.

Currently, single-cell C₄ photosynthesis has been reported in four terrestrial plant species, Bienertia cycloptera, B. sinuspersici, B. kavirense and Suaeda aralocaspica, of family Chenopodiaceae. These species possess novel mechanisms of C₄ photosynthesis through spatial partitioning of organelles and key enzymes in distinct cytoplasmic domains within single chlorenchyma cells. Anatomical and biochemical studies have shown that the three Bienertia species and S. aralocaspica utilize biochemical and organellar compartmentation to achieve the equivalent spatial separation of Kranz anatomy but within a single photosynthetic cell. These discoveries have challenged the paradigm for C₄ photosynthesis in terrestrial plants which had suggested for more than 40 years that the Kranz feature was indispensably required for its C₄ function. In this review, we focus on the recent progress in understanding the cellular and molecular mechanisms that control the spatial relationship of organelles in these unique single-cell C₄ systems. The demonstrated interaction of dimorphic chloroplasts with microtubules and actin filaments has shed light on the importance of these cytoskeleton components in the intracellular partitioning of organelles. Future perspectives on the potential function of the cytoskeleton in targeting gene products to specific subcellular compartments are discussed.

Carbon (C) and nitrogen (N) are two essential nutrients affecting plant growth and development. Plants are non-motile organisms and have evolved highly sophisticated and complex sensing and signaling mechanisms to respond to the dynamic changes of C and N nutrients in their surroundings. C and N metabolism are tightly coordinated to maintain intracellular C/N homeostasis. However, the regulatory mechanism underlying C/N coordination and balancing in plants remains to be elucidated. It has been suggested that C and N metabolism are modulated by the interaction of C signaling with N signaling or by C/N ratio signaling. This review focuses on cell signaling studies that provide insight into the regulation mechanism of C/N balancing in plants.

Environmental and food safety concerns over transgenic plants have hampered commercial applications of transgenic plant technology worldwide. A recently developed transgene deletion technology, named gene deletor technology, may be used to eliminate all transgenes from pollen, seeds, fruits or other organs when functions of transgenes are no longer needed or their presence may cause concerns. In this review, I will briefly describe the principle of the gene deletor technology with major supporting experimental data. I will also explain main characteristics and requirements of the gene deletor technology. Finally, I will discuss the gene deletor technology in the context of how it may be used to alleviate environmental and food safety concerns over transgenic plants in vegetatively and sexually propagated plants, to prevent volunteer transgenic plants, to protect proprietary transgenic technologies, and to allow farmers to reuse their harvested seeds for future planting.

Phosphorylation is one of the most common post translational modifications (PTM), participating in a large number of processes to regulate cellular functions. Phosphorylation is also one of the key factors in the origin and development of cancer. The rapid development of mass spectrometric-based phosphoproteomic technologies has made it possible for high-throughput identification and quantification of phosphorylation events. In this review, we provide a general introduction and summary of the achievements made in mass spectrometry based phosphoproteomic research, including the approaches for phosphopeptide identification and quantification, as well as instrumentation and data interpretation methods. We also review some discoveries in cancer research made possible by phosphoproteomic analysis technologies.

Throughout the animal kingdom, Wnt-triggered signal transduction pathways play fundamental roles in embryonic development and tissue homeostasis. Wnt proteins are modified as glycolipoproteins and are secreted into the extracellular environment as morphogens. Recent studies on the intracellular trafficking of Wnt proteins demonstrate multiple layers of regulation along its secretory pathway. These findings have propelled a great deal of interest among researchers to further investigate the molecular mechanisms that control the release of Wnts and hence the level of Wnt signaling. This review is dedicated to Wntless, a putative G-protein coupled receptor that transports Wnts intracellularly for secretion. Here, we highlight the conclusions drawn from the most recent cellular, molecular and genetic studies that affirm the role of Wntless in the secretion of Wnt proteins.