TRANSPARENT TESTA GLABRA1 regulates high-intensity blue light-induced phototropism by reducing CRYPTOCHROME1 levels.

The asymmetrical distribution of auxin supports high intensity blue light (HBL)-mediated phototropism. Flavonoids, secondary metabolites induced by blue light and TRANSPARENT TESTA GLABRA1 (TTG1), alter auxin transport. However, the role of TTG1 in HBL-induced phototropism in Arabidopsis (Arabidopsis thaliana) remains unclear. We found that TTG1 regulates HBL-mediated phototropism. HBL-induced degradation of CRYPTOCHROME 1 (CRY1) was repressed in ttg1-1, and depletion of CRY1 rescued the phototropic defects of the ttg1-1 mutant. Moreover, overexpression of CRY1 in a cry1 mutant background led to phototropic defects in response to HBL. These results indicated that CRY1 is involved in the regulation of TTG1-mediated phototropism in response to HBL. Further investigation showed that TTG1 physically interacts with CRY1 via its N-terminus and that the added TTG1 promotes the dimerization of CRY1. The interaction between TTG1 and CRY1 may promote HBL-mediated degradation of CRY1. TTG1 also physically interacted with blue light inhibitor of cryptochrome 1 (BIC1) and Light-Response Bric-a-Brack/Tramtrack/Broad 2 (LRB2), and these interactions either inhibited or promoted their interaction with CRY1. Exogenous gibberellins (GA) and auxins, two key plant hormones that crosstalk with CRY1, may confer the recovery of phototropic defects in the ttg1-1 mutant and CRY1-overexpressing plants. Our results revealed that TTG1 participates in the regulation of HBL-induced phototropism by modulating CRY1 levels, which are coordinated with GA or IAA signaling.

Cryptochrome-mediated hypocotyl phototropism was regulated antagonistically by gibberellic acid and sucrose in Arabidopsis.

Both phototropins (phot1 and phot2) and cryptochromes (cry1 and cry2) were proven as the Arabidopsis thaliana blue light receptors. Phototropins predominately function in photomovement, and cryptochromes play a role in photomorphogenesis. Although cryptochromes have been proposed to serve as positive modulators of phototropic responses, the underlying mechanism remains unknown. Here, we report that depleting sucrose from the medium or adding gibberellic acids (GAs) can partially restore the defects in phototropic curvature of the phot1 phot2 double mutants under high-intensity blue light; this restoration does not occur in phot1 phot2 cry1 cry2 quadruple mutants and nph3 (nonphototropic hypocotyl 3) mutants which were impaired phototropic response in sucrose-containing medium. These results indicate that GAs and sucrose antagonistically regulate hypocotyl phototropism in a cryptochromes dependent manner, but it showed a crosstalk with phototropin signaling on NPH3. Furthermore, cryptochromes activation by blue light inhibit GAs synthesis, thus stabilizing DELLAs to block hypocotyl growth, which result in the higher GAs content in the shade side than the lit side of hypocotyl to support the asymmetric growth of hypocotyl. Through modulation of the abundance of DELLAs by sucrose depletion or added GAs, it revealed that cryptochromes have a function in mediating phototropic curvature.

NITRIC OXIDE-ASSOCIATED PROTEIN1 (AtNOA1) is essential for salicylic acid-induced root waving in Arabidopsis thaliana.

Root waving responses have been attributed to both environmental and genetics factors, but the potential inducers and transducers of root waving remain elusive. Thus, the identification of novel signal elements related to root waving is an intriguing field of research. Genetic, physiological, cytological, live cell imaging, and pharmacological approaches provide strong evidence for the involvement of Arabidopsis thaliana NITRIC OXIDE-ASSOCIATED PROTEIN1 (AtNOA1) in salicylic acid (SA)-induced root waving. SA specially induced root waving, with an overall decrease in root elongation in A. thaliana, and this SA-induced response was disrupted in the Atnoa1 mutant, as well as in nonexpresser of pathogenesis-related genes 1 (npr1), which is defective in SA-mediated plant defense signal transduction, but not in npr3/4 single and double mutants. The expression assays revealed that the abundance of AtNOA1 was significantly increased by application of SA. Genetic and pharmacological analyses showed that SA-induced root waving involved an AtNOA1-dependent Ca(2+) signal transduction pathway, and PIN-FORMED2 (PIN2) -based polar auxin transport possibly plays a crucial role in this process. Our work suggests that SA signaling through NPR1 and AtNOA1 is involved in the control of root waving, which provides new insights into the mechanisms that control root growth behavior on a hard agar surface.

Hydrogen peroxide mediates high-intensity blue light-induced hypocotyl phototropism of cotton seedlings.

Phototropism is a classic adaptive growth response that helps plants to enhance light capture for photosynthesis. It was shown that hydrogen peroxide (H2O2) participates in the regulation of blue light-induced hypocotyl phototropism; however, the underlying mechanism is unclear. In this study, we demonstrate that the unilateral high-intensity blue light (HBL) could induce asymmetric distribution of H2O2 in cotton hypocotyls. Disruption of the HBL-induced asymmetric distribution of H2O2 by applying either H2O2 itself evenly on the hypocotyls or H2O2 scavengers on the lit side of hypocotyls could efficiently inhibit hypocotyl phototropic growth. Consistently, application of H2O2 on the shaded and lit sides of the hypocotyls led to reduced and enhanced hypocotyl phototropism, respectively. Further, we show that H2O2 inhibits hypocotyl elongation of cotton seedlings, thus supporting the repressive role of H2O2 in HBL-induced hypocotyl phototropism. Moreover, our results show that H2O2 interferes with HBL-induced asymmetric distribution of auxin in the cotton hypocotyls. Taken together, our study uncovers that H2O2 changes the asymmetric accumulation of auxin and inhibits hypocotyl cell elongation, thus mediating HBL-induced hypocotyl phototropism.

Functional Analysis of MAX2 in Phototropins-Mediated Cotyledon Flattening in Arabidopsis.

Phototropins (phot1 and phot2) are blue-light receptors that control cotyledon flattening and positioning under strong light; however, their functional redundancy restricts our understanding of the specific roles of phot2. To identify the factors responsible for phot2-dependent cotyledon flattening and growth, we screened for light-insensitive mutants among mutagenized phot1 mutants in Arabidopsis thaliana. The double mutant phot1 lea1 (leaf expansion associated 1), which is defective in cotyledon flattening and positioning but not the phototropic response was selected. This mutant phenotype could be alleviated by constitutively expressing MORE AXILLARY GROWTH 2 (MAX2), indicating that LEA1 was allelic to MAX2. The max2 mutants (max2-2 and max2-3) are defective in cotyledon flattening, which is similar to that of the phot1 phot2 mutants. Moreover, the amounts of MAX2 transcripts are inhibited in leaves of phot1 mutant. However, the additional disruption of PHOT1 gene in max2-2 or max2-3 did not affect their phenotype, including MAX2-mediated inhibition of hypocotyl elongation. By contrast, phototropins-mediated hypocotyl phototropism was not regulated by MAX2. Together, these results suggest that cotyledon flattening was mediated by both phototropins and MAX2 signaling, but the relationship between two pathways need further study.

[Clinical efficiency of interventional therapy on internal carotid-posterior communicating artery aneurysm].

OBJECTIVE: To evaluate the effect of endovascular embolization of internal carotid-posterior communicating artery (IC-PC) aneurysm. METHODS: 145 patients with IC-PC aneurysms underwent endovascular embolization through the microcatheter under digital subtraction angiography (DSA). Of the 145 cases, 55 patients with 62 aneurysms were embolized by mechanical detachable spiral (MDS) and 90 patients with 106 aneurysms were embolized by Guglielmi detachable coil (GDC) or electrical detachable coil (EDC). RESULTS: 168 aneurysms in 145 patients, 96 of which with 100% embolization, 45 with 95% embolization, 15 with 90% embolization, and 12 with less than 90% embolization, were embolized successfully. During the surgery, aneurysm rupture occurred in 3 cases, cerebral vasospasm in 5, and cerebral infarction in 1 case. 118 cases were cured, 23 improved, and 3 died. 17 patients were followed-up by DSA, 3 aneurysms recurred and 2 were totally embolized with EDC for the second time. CONCLUSION: Endovascular embolization is a safe and effective therapeutic method for IC-PC aneurysm.

[Mechanism of Ca2+ on the hyperthermia-induced apoptosis of rat hippocampal neurons in vitro].

OBJECTIVE: To study the mechanism of Ca(2+) on the apoptosis induced by hyperthermia in neonate rat hippocampal neurons to provide the applicative evidence of dantrolene for preventing brain injuries. METHODS: Dantrolene, Ca(2+) specific blocking agent, was used in the hyperthermia-induced apoptosis of primary hippocampal neurons in vitro to observe its effect on the apoptosis, fluorescent intensity, and dynamic change of Ca(2+) by flowcytometry and laser confocal microscopy. RESULTS: The rate of apoptosis was decreased significantly after hyperthermia treatment by dantrolene sodium. The intracellular Ca(2+) fluorescent intensity in 42 degrees C treatment group (107.35 +/- 6.0) was significantly lower than that in control group (159.12 +/- 33.8). The concentration of Ca(2+) began to decrease 20 approximately 25 s after adding dantrolene sodium, and reached the lowest level about 50 s later, and then kept lower than the basal level. CONCLUSION: Dantrolene sodium has an important protective effect on hippocampal neurons apoptosis induced by hyperthermia and may have some applicative value of preventing heat-induced brain injury.

[Changes in Ca2+ concentration mediated by N-methyl-D-aspartate receptor in PO/AH neurons of anoxic SD rats].

OBJECTIVE: To study the changes of Ca2+ concentration mediated by N-methyl-D-aspartate (NMDA) receptor in the neurons in the preoptic area/anterior hypothalamus (PO/AH) of anoxic SD rats by investigating the properties of NMDA receptor. METHODS: The effects of NMDA receptor agonist NMDA and antagonist vaproic acid (VPA) on the [Ca2+]i in PO/AH neurons were observed in SD rats with anoxia. RESULTS: Under normal condition, the fluorescencet ratio was 0.95, which increased obviously in response to treatment with NMDA at 40 s and reached the peak value, 2.054, after 25 s with an increment of (109+/-52) %. After the addition of the agonist, the peak value reached 3.783 in 30 s and maintained the high level. The concentration of Ca2+ increased by (286+/-91) % after the treatment with NMDA. While in the anoxia group, the concentration of Ca2+ decreased by (103+/-45)% after the addition of VPA. CONCLUSIONS: The increase in the concentration of Ca2+ results predominantly from the opening of NMDA receptor channel which allows Ca2+ influx. VPA may decrease the activity of NMDA receptor to reduce the Ca2+ concentration for the protection of the neurons against anoxia.

[Expression of TGFbeta1 and its type I receptors ALK1 and ALK5 mRNA in brain arteriovenous malformation].

OBJECTIVE: To explore the expression of transforming growth factor beta1 (TGFbeta1) and its type I receptors activin-like kinase 1 (ALK1) and ALK5 mRNA in the development of brain arteriovenous malformation (BAVM). METHODS: The mRNA expressions of TGFbeta1, ALK1and ALK5 were detected with semiquantitative RT-PCR in patients with BAVM. RESULTS: The expressions of TGFbeta1 and ALK5 mRNA increased significantly in BAVM, and their relative expression quantity were 0.777-/+0.047 and 0.585-/+0.074, respectively. However, ALK1 mRNA expression declined significantlies with a relative expression of 0.173-/+0.044 in comparison with the control group (0.720-/+0.098, P<0.01). CONCLUSION: The balance of TGFbeta1 and its type I receptors ALK1 and ALK5 mRNA expressions may play important role in the development of BAVM.