Cytosolic Invertase-Mediated Root Growth Is Feedback Regulated by a Glucose-Dependent Signaling Loop.

The disaccharide Suc cannot be utilized directly; rather, it is irreversibly hydrolyzed by invertase to the hexoses Glc and Fru to shape plant growth. In this context, Glc controls the stability of the transcription factor Ethylene-Insensitive3 (EIN3) via the function of Hexokinase1 (HXK1), a Glc sensor. Thus, invertase, especially the major neutral cytosolic invertase (CINV), constitutes a key point of control for plant growth. However, the cognate regulatory mechanisms that modulate CINV activity remain unclear. Here, we demonstrate that in Arabidopsis (Arabidopsis thaliana), EIN3 binds directly to both the promoters of Production of Anthocyanin Pigment1 (PAP1) and Phosphatidylinositol Monophosphate 5-Kinase 9 (PIP5K9), repressing and enhancing, respectively, their expression. Subsequently, PAP1 binds directly to and promotes transcription of the Cytosolic Invertase1 (CINV1) promoter, while PIP5K9 interacts with and negatively regulates CINV1. The accumulated CINV1 subsequently hydrolyzes Suc, releasing the sequestered signaling cue, Glc, which has been shown to negatively regulate the stability of EIN3 via HXK1. We conclude that a CINV1-Glc-HXK1-EIN3-PAP1/PIP5K9-CINV1 loop contributes to the modulation of CINV1 activity regulating root growth by Glc signaling.

Molecular Mechanism Underlying the Effect of the Intraspecific Alternation of Seed Size on Plant Drought Tolerance.

In crop plants, the yield loss caused by drought exceeds the losses resulting from other adverse environment stresses. In numerous plant species, seedling establishment is positively correlated with the initial seed size under drought stress conditions. In intra- and interspecies, plants with large seeds can withstand water deficiency stresses, whereas those with small seeds are efficient colonizers as a result of their ability to produce more seeds. Therefore, larger initial seeds confer more drought resistance on germinating seedlings. Although this phenomenon has been observed by evolutionary biologists and ecologists, the correlation of initial seed size with the drought resistance of seedlings/plants is not well-reviewed and characterized. Furthermore, the related molecular mechanisms are unknown. Understanding these mechanisms will benefit future breeding or design strategies to increase crop yields. In the present review, we focus on recent research to analyze the genetic factors of plants/crops involved in the regulation of seed size and drought tolerance and their corresponding signal transduction pathways. Several signaling pathways that determine plant drought tolerance through influencing the initial seed size are identified. Such pathways include those that are involved in mitogen-activated protein kinase, abscisic acid, brassinosteroids, and several transcription factors and sugar signaling pathways.

New Insights into the Molecular Mechanism Underlying Seed Size Control under Drought Stress.

In higher plants, seed size is an important parameter and agricultural trait in many aspects of evolutionary fitness. The loss of water-deficiency-induced crop yield is the largest among all natural hazards. Under water-deficient stress, the most prevalent response to terminal stress is to accelerate the early arrest of floral development and, thereby, to accelerate fruit/seed production, which consequently reduces seed size. This phenomenon is well-known, but its molecular mechanism is not well-reviewed and characterized. However, increasing evidence have indicated that water-deficient stress is always coordinated with three genetic signals (i.e., seed size regulators, initial seed size, and fruit number) that decide the final seed size. Here, our review presents new insights into the mechanism underlying cross-talk water-deficient stress signaling with three genetic signals controlling final seed size. These new insights may aid in preliminary screening, identifying novel genetic factors and future design strategies, or breeding to increase crop yield.

HOXA10 knockdown inhibits proliferation, induces cell cycle arrest and apoptosis in hepatocellular carcinoma cells through HDAC1.

BACKGROUND: Homeobox A10 (HOXA10) has been implicated in the development and progression of various human cancers. However, the precise biological functions of HOXA10 in hepatocellular carcinoma (HCC) have not been defined. METHODS: In this study, we examined mRNA expression by quantitative real-time PCR (qRT-PCR) of HOXA10 as well as histone deacetylase (HDAC) and protein levels by Western blot of HOXA10, HDAC1, Cyclin D1, proliferating cell nuclear antigen (PCNA), Survivin and p53 acetylation in HCC tissues and cell lines. We also assessed cell proliferation using Cell Counting Kit-8 (CCK-8) and analyzed cell cycle by flow cytometry. Furthermore, tumor growth of HCC cells in vivo was monitored using the nude mouse xenograft model. Finally, HDAC1 promoter activity and binding in HCC cell lines were detected by luciferase reporter assay and chromatin immunoprecipitation (ChIP), respectively. RESULTS: We uncovered the elevated expression of HOXA10 in HCC tissues compared to adjacent normal liver tissues. RNA interference-mediated knockdown of HOXA10 inhibited HCC cell proliferation both in vitro and in vivo. HOXA10 knockdown also induced cell cycle arrest at G0/G1 phase and apoptosis, which were accompanied with the reduced expression of Cyclin D1, PCNA and Survivin. Notably, HOXA10 knockdown enhanced p53 acetylation (Lys382), which is crucial to the activation of p53. Likewise, HOXA10 knockdown suppressed the transcription of HDAC1, a potential deacetylase for p53. In line with these observations, HDAC1 downregulation abrogated the effects of HOXA10 overexpression on proliferation, cell cycle progression, apoptosis and p53 acetylation, indicating the role of HDAC1 in mediating HOXA10 functions. CONCLUSION: Our results demonstrate that HOXA10 knockdown inhibits proliferation, induces cell cycle arrest and apoptosis in HCC cells by regulating HDAC1 transcription.

Sucrose Signaling Regulates Anthocyanin Biosynthesis Through a MAPK Cascade in Arabidopsis thaliana.

Anthocyanin accumulation specifically depends on sucrose (Suc) signaling. However, the molecular basis of this process remains unknown. In this study, in vitro pull-down assays identified ETHYLENE-INSENSITIVE3 (EIN3), a component of both sugar signaling or/and metabolism. This protein interacted with YDA, and the physiological relevance of this interaction was confirmed by in planta co-immunoprecipitation, yeast two-hybrid (Y2H) assay, and bimolecular fluorescence complementation. Ethylene insensitive3-like 1 (eil1) ein3 double-mutant seedlings, but not ein3-1 seedlings, showed anthocyanin accumulation. Furthermore, ein3-1 suppressed anthocyanin accumulation in yda-1 plants. Thus, EMB71/YDA-EIN3-EIL1 may form a sugar-mediated gene cascade integral to the regulation of anthocyanin accumulation. Moreover, the EMB71/YDA-EIN3-EIL1 gene cascade module directly targeted the promoter of Transparent Testa 8 (TT8) by direct EIN3 binding. Collectively, our data inferred a molecular model where the signaling cascade of the YDA-EIN3-TT8 appeared to target TT8 via EIN3, thereby modulating Suc signaling-mediated anthocyanin accumulation.