SummaryThe growth and yield of many crops, including cotton, are affected by water deficit. Cotton has evolved drought specific as well as general morpho‐physiological, biochemical and molecular responses to drought stress, which are discussed in this review. The key physiological responses against drought stress in cotton, including stomata closing, root development, cellular adaptations, photosynthesis, abscisic acid (ABA) and jasmonic acid (JA) production and reactive oxygen species (ROS) scavenging, have been identified by researchers. Drought stress induces the expression of stress‐related transcription factors and genes, such as ROS scavenging, ABA or mitogen‐activated protein kinases (MAPK) signalling genes, which activate various drought‐related pathways to induce tolerance in the plant. It is crucial to elucidate and induce drought‐tolerant traits via quantitative trait loci (QTL) analysis, transgenic approaches and exogenous application of substances. The current review article highlights the natural as well as engineered drought tolerance strategies in cotton.

Upconversion nanoparticle (UCNP)-mediated photodynamic therapy has shown great effectiveness in increasing the tissue-penetration depth of light to combat deep-seated tumors. However, the inevitable phototoxicity to normal tissues resulting from the lack of tumor selectivity remains as a major challenge. Here, the development of tumor-pH-sensitive photodynamic nanoagents (PPNs) comprised of self-assembled photosensitizers grafted pH-responsive polymeric ligands and UCNPs is reported. Under neutral pH conditions, photosensitizers aggregated in the PPNs are self-quenched; however, upon entry into a tumor microenvironment with lower pH, the PPNs not only exhibit enhanced tumor-cell internalization due to charge reversal but also are further disassembled into well-dispersed nanoparticles in the endo/lysosomes of tumor cells, enabling the efficient activation of photosensitizers. The results demonstrate the attractive properties of both UCNP-mediated deep-tissue penetration of light and high therapeutic selectivity in vitro and in vivo.

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One of the key problems hindering skin repair is the deficiency of dermal vascularization and difficulty of epidermis regeneration, which makes it challenging to fabricate scaffolds that can biologically fulfill the requirements for skin regeneration. To overcome this problem, three-dimensional printing was used to fabricate a gelatin-sulfonated silk composite scaffold that was incorporated with basic fibroblast growth factor 2 (FGF-2) through binding with a sulfonic acid group (SO3) (3DG-SF-SO3-FGF). The efficacy and mechanism by which the 3DG-SF-SO3-FGF scaffolds promote skin regeneration were investigated both within in vitro cell culture and in vivo with a full-thickness skin defect model. The histological results showed that the gelatin-sulfonated silk composite scaffolds promoted granulation, and that incorporation of FGF-2 significantly enhanced the regeneration of skin-like tissues after implantation in rat skin defects for 14 and 28 days. Further investigations demonstrated that 3DG-SF-SO3-FGF scaffolds might stimulate dermal vascularization. These findings thus suggest that incorporation of FGF-2 into the 3D printed scaffolds is a viable strategy for enhancing skin regeneration.

The cambium and procambium generate the majority of biomass in vascular plants. These meristems constitute a bifacial stem cell population from which xylem and phloem are specified on opposing sides by positional signals. The PHLOEM INTERCALATED WITH XYLEM (PXY) receptor kinase promotes vascular cell division and organization. However, how these functions are specified and integrated is unknown. Here, we mapped a putative PXY-mediated transcriptional regulatory network comprising 690 transcription factor-promoter interactions in Arabidopsis (Arabidopsis thaliana). Among these interactions was a feedforward loop containing transcription factors WUSCHEL HOMEOBOX RELATED14 (WOX14) and TARGET OF MONOPTEROS6 (TMO6), each of which regulates the expression of the gene encoding a third transcription factor, LATERAL ORGAN BOUNDARIES DOMAIN4 (LBD4). PXY signaling in turn regulates the WOX14, TMO6, and LBD4 feedforward loop to control vascular proliferation. Genetic interaction between LBD4 and PXY suggests that LBD4 marks the phloem-procambium boundary, thus defining the shape of the vascular bundle. These data collectively support a mechanism that influences the recruitment of cells into the phloem lineage, and they define the role of PXY signaling in this context in determining the arrangement of vascular tissue.

SummaryPyruvate kinase type M2 (PKM2) has been reported to be involved in aerobic glycolysis and cell growth in various tumors. However, the expression pattern of PKM2 in colorectal cancer (CRC) and the correlation between PKM2 expression and CRC remains unclear. The aim of this study is to investigate PKM2 expression and its possible role in CRC. We found that expression of PKM2 was increased in CRC and the increased PKM2 expression was associated with later stage and lymph metastasis of the tumors. Knockdown of PKM2 suppressed the aerobic glycolysis and decreased lactate production of colon cancer RKO cells. Knockdown of PKM2 repressed proliferation and migration of the cells. Inhibition of PKM2 suppressed xenograft tumor growth of RKO cells in vivo. These results suggest that the expression of PKM2 plays a critical role in development of CRC, and it may provide a growth advantage for colon cancer cells. Thus, PKM2 might be a potential therapeutic target for CRC.2012 IUBMB IUBMB Life, 64(9): 775-782, 2012

WRKY transcription factors are transcriptional regulators of signaling pathways involved in biotic and abiotic stress responses. In this study, we report that ectopic expression of the GhWRKY6-like gene significantly improved salt tolerance in Arabidopsis thaliana while silencing the GhWRKY6-like increase the sensitivity to abiotic stresses in cotton. GhWRKY6-like was localized to the nucleus. Expression of GhWRKY6-like was remarkably induced by salt, polyethylene glycol (PEG) and abscisic acid (ABA) treatments. For further characterization, the GhWRKY6-like gene was cloned and transformed into Arabidopsis. Our findings showed that the germination rate and root length were significantly improved in plants overexpressing GhWRKY6-like vs wild type (WT) under salt, mannitol and ABA treatments. Additionally, the overexpressing lines showed greater salt tolerance than WT plants in soil. In addition, overexpressing plants accumulated less H O and malondialdehyde (MDA), while higher proline content, superoxide dismutase (SOD) and peroxidase (POD) activities were detected under salt and osmotic stresses. In contrast, virus-induced gene silencing (VIGS) of GhWRKY6-like in cotton showed enhanced sensitivity compared to WT plants during salt and drought stresses. Additionally, expression analysis of stress-responsive genes in GhWRKY6-like Arabidopsis revealed that there was increased expression of genes involved in the ABA signaling pathway (AtABF4, AtABI5 and AtMYC2) and osmotic stress (AtSOS2, AtRD29a and AtRD29b). Our results revealed that GhWRKY6-like enhanced salt tolerance in Arabidopsis by scavenging reactive oxygen species and regulating the ABA signaling pathway. We suggest that overexpression of the GhWRKY6-like gene in cotton will enhance tolerance against salt, drought and osmotic stresses.

TNF receptor (TNFR)-associated factor TRAF6 is a key activator of NF-kB, playing a critical role in the regulation of innate immune responses and their connection to adaptive immune responses. TRAF6 interactions determine receptor-induced cell death versus survival. TRAF6 has been implicated in cancer but its contributions have not been investigated deeply. In this study, we show that TRAF6 upregulates expression of hypoxia-inducible factor (HIF)-1a. TRAF6 affects HIF-1a protein levels but has little effect on mRNA level. TRAF6 increases HIF-1a protein independent of oxygen. We found that TRAF6 binds HIF-1a and mediates its K63-linked polyubiquitination. The E3 ligase activity of TRAF6 was required to increase HIF-1a protein levels. Finally, we showed that TRAF6 promoted tumor angiogenesis and growth. Our results reveal how TRAF6 functions to upregulate HIF-1a expression and promote tumor angiogenesis. Cancer Res; 73(15);