Search

Key message: Identification and characterization of a semi-dwarfing gene ds-3 encoding a mutant DELLA protein regulating plant height through gibberellin signaling pathway. Abstract: Lodging is one of the most important factors causing severe yield loss in oilseed rape. Utilization of semi-dwarf varieties has been proved the most effective way to increase lodging resistance and yield in many crops. To develop semi-dwarf germplasm in oilseed rape, we identified a semi-dwarf mutant ds-3 which showed a reduced response to phytohormones gibberellins (GAs). Genetic analysis indicated the dwarfism was controlled by a single semi-dominant gene, ds-3. The DS-3 gene was mapped to a genomic region on chromosome C07, which is syntenic to the region of a previously identified semi-dwarf gene ds-1 ( BnaA06.RGA). In this region, DS-3 ( BnaC07.RGA) gene was identified to encode a DELLA protein that functions as a repressor in GA signaling pathway. A substitution of proline to leucine was identified in ds-3 in the conserved VHYNP motif, which is essential for GA-dependent interaction between gibberellin receptor GID1 and DELLA proteins. Segregation analysis in the F population derived from the cross between ds-1 and ds-3 demonstrated that BnaA06.RGA displayed a stronger effect on plant height than BnaC07.RGA, indicating that different RGA genes may play different roles in stem elongation. In addition to BnaA06.RGA and BnaC07.RGA, two more RGA genes ( BnaA09.RGA and BnaC09.RGA) were identified in the Brassica napus ( B. napus) genome. Reverse-transcription polymerase chain reaction (RT-PCR) and yeast two-hybrid (Y2H) assays suggest that both BnaA09.RGA and BnaC09.RGA are transcribed in leaves and stems and can mediate GA signaling in vivo. These genes represent potential targets for screening ideal semi-dwarfing alleles for oilseed rape breeding. [ABSTRACT FROM AUTHOR]

Abstract: Activated mTOR was implicated to play a role in the carcinogenesis of nasopharyngeal carcinoma (NPC). However, the mechanism of activated mTOR/Complex1(mTORC1) signaling pathway in NPC development has not been well established. In this study, we correlated the expression of mTORC1 signal molecules and Cyclin D1 in NPC. We also investigated the effect of blocking mTORC1 signal with rapamycin and mTOR siRNA on Cyclin D1 expression in CNE-2 cells, as well as cell apoptosis and viability. We found a positive association of mTORC1 signal molecules and Cyclin D1 in NPC. Also, we found blockage mTORC1 inhibited Cyclin D1 expression in CNE-2 cells and enhanced cell apoptosis. Our results suggested that mTORC1 signal pathway might be a potential target for NPC therapy. [Copyright &y& Elsevier]

Summary Among the myriad cues that constantly inform plant growth and development, mechanical forces are unique in that they are an intrinsic result of cellular turgor pressure and also imposed by the environment [ 1 ]. Although the key role of mechanical forces in shaping plant architecture from the cellular level to the level of organ formation is well established [ 1–4 ], the components of the early mechanical signal transduction machinery remain to be defined at the molecular level. Here, we show that an Arabidopsis mutant lacking the receptor-like kinase FERONIA (FER) shows severely altered Ca 2+ signaling and growth responses to different forms of mechanical perturbation. Ca 2+ signals are either abolished or exhibit qualitatively different signatures in feronia ( fer ) mutants exposed to local touch or bending stimulation. Furthermore, mechanically induced upregulation of known touch-responsive genes is significantly decreased in fer mutants. In addition to these defects in mechanical signaling, fer mutants also exhibit growth phenotypes consistent with impaired mechanical development, including biased root skewing, an inability to penetrate hard agar layers, and abnormal growth responses to impenetrable obstacles. Finally, high-resolution kinematic analysis of root growth revealed that fer mutants show pronounced spatiotemporal fluctuations in root cell expansion profiles with a timescale of minutes. Based on these results, we propose that FER is a key regulator of mechanical Ca 2+ signaling and that FER-dependent mechanical signaling functions to regulate growth in response to external or intrinsic mechanical forces. [ABSTRACT FROM AUTHOR]

Metastasis is the leading cause of deaths in patients with breast cancer. Benzo[a]pyrene is a cumulative carcinogen and ubiquitous environmental pollutant with potent carcinogenic properties. As we report here, we established an accumulative mouse model mimicking the cumulative effects of benzo[a]pyrene exposure in human breast carcinogenesis. Our focus was on elucidating the mechanisms by which benzo[a]pyrene contributes to the process of breast cancer metastasis. Our study indicated that benzo[a]pyrene increased the migration of breast cancer cells both in vitro and in vivo . Specifically, we demonstrated that benzo[a]pyrene enhances breast cancer cell migration and invasion by up-regulating ROS-induced ERK signaling, leading to the activation of matrix metalloproteinases 9. Our results suggest that benzo[a]pyrene-induced mammary gland cancer metastasis is an important and intricate process facilitated by cumulative benzo[a]pyrene exposure leading to activation of the ROS-ERK-MMP9 signaling pathway. [ABSTRACT FROM AUTHOR]