Phot1 and phot2 mediate blue light regulation of stomatal opening.

The stomatal pores of higher plants allow for gaseous exchange into and out of leaves. Situated in the epidermis, they are surrounded by a pair of guard cells which control their opening in response to many environmental stimuli, including blue light. Opening of the pores is mediated by K(+) accumulation in guard cells through a K(+) channel and driven by an inside-negative electrical potential. Blue light causes phosphorylation and activation of the plasma membrane H(+)-ATPase that creates this potential. Thus far, no blue light receptor mediating stomatal opening has been identified, although the carotenoid, zeaxanthin, has been proposed. Arabidopsis mutants deficient in specific blue-light-mediated responses have identified four blue light receptors, cryptochrome 1 (cry1), cryptochrome 2 (cry2), phot1 and phot2. Here we show that in a double mutant of phot1 and phot2 stomata do not respond to blue light although single mutants are phenotypically normal. These results demonstrate that phot1 and phot2 act redundantly as blue light receptors mediating stomatal opening.

Arabidopsis NPL1: a phototropin homolog controlling the chloroplast high-light avoidance response.

Chloroplasts relocate their positions in a cell in response to the intensity of incident light, moving to the side wall of the cell to avoid strong light, but gathering at the front face under weak light to maximize light interception. Here, Arabidopsis thaliana mutants defective in the avoidance response were isolated, and the mutated gene was identified as NPL1 (NPH-like 1), a homolog of NPH1 (nonphototropic hypocotyl 1), a blue light receptor used in phototropism. Hence, NPL1 is likely a blue light receptor regulating the avoidance response under strong light.

Glucose and lipid metabolism during long-term antihypertensive treatment with indapamide in non-insulin-dependent diabetic patients.

Thirty-nine patients with diabetes and hypertension were treated with indapamide for 24 weeks to study the effects of that drug on glucose and lipid metabolism. The drug was administered at a dose of 2 mg once per day in the morning as a single drug (26 patients) or in combination with other antihypertensive drugs (13 patients), including calcium antagonists, angiotensin-converting enzyme inhibitors, an alpha-blocker, or a beta-blocker. Blood pressure was reduced in both groups during treatment, and no alteration of glycemic control or lipid metabolism was observed. One patient complained of a mild headache, but treatment was continued. The results indicate that indapamide is useful for the long-term treatment of hypertension in diabetic patients, either alone or in combination with other antihypertensive agents.

Effects of chlorinated benzenes of the activities of delta-aminolevulinic acid synthetase and heme oxygenase and on the content of hemoprotein in the liver of rats.

Effects of chlorinated benzenes on the activities of delta-aminolevulinic acid (delta-ALA) synthetase and heme oxygenase, the rate-limiting enzyme in heme biosynthesis and degradation respectively, and on the incorporation of 3H-delta-ALA into hemoprotein in the liver of male rats were investigated. Monochlorobenzene (MCB) and 1,2,4-trichlorobenzene(TRCB) stimulated significantly the activities of above both hepatic enzymes. After a single injection of 200 mg/kg, heme oxygenase activity was enhanced rapidly and sustained markedly for at least 48 hr by MCB treatment, while that was also enhanced but restored nearly to control levels at 48 hr by TRCB. delta-ALA synthetase activity was once decreased at 6 hr and restored within 12 hr and then reached peak levels (about 2--3 times to control levels) at 24 hr by MCB or TRCB treatment. However, this activity was sustained for 48 hr by TRCB treatment, whereas returned again to nearly control levels by MCB at 48 hr. Cytochrome P-450 content at 48 hr was significantly decreased by MCB (63% to control), in contrast, increased by TRCB (200% to control). When MCB or TRCB injected once daily throughout the study, biphasic disappearance of radioactivity incorporated into CO-binding particles was shown in control and MCB- or TRCB-treated rats. The half-life of the fast phase was about 8 hr in control and about 6 or 13 hr in MCB- or TRCB-treated rats respectively.

Hydrolysis of aryl beta-maltotriosides by sweet potato beta-amylase and soybean beta-amylase.

Sweet potato beta-amylase [EC 3.2.1.2, alpha 1,4-D-glucan maltohydrolase]-catalyzed hydrolyses of aryl beta-maltotriosides with substituents, NO2-, Cl-, and Br- at the o-, m-, and p-positions in the phenyl ring were studied at pH 4.8 and 25 degrees C. The hydrolyses of a few of the maltotriosides by soybean beta-amylase [EC 3.2.1.2, alpha-1,4-D-glucan maltohydrolase] were also studied at pH 5.4 and 25 degrees C. It was found that the aryl beta-maltotriosides were preferentially hydrolyzed into maltose and aryl beta-D-glucosides by both beta-amylases. The Michaelis constant Km and the molecular activity ko were determined for the hydrolyses of these maltotriosides and compared with those of maltotriose and maltotetraose. Aryl beta-maltotriosides were more rapidly hydrolyzed than maltotriose by a factor of 30--80, and more slowly hydrolyzed than maltotetraose by a factor of 10--30, depending on the kinds of substituents. The rapid hydrolysis of aryl beta-maltotrioside as compared with maltotriose may be due to the interaction of an aryl group with the subsite of beta-amylase. This is in contrast with glucoamylase [EC 3.2.1.3, alpha-1,4-D-glucan glucohydrolase] of Rhizopus niveus-catalyzed hydrolysis of phenyl beta-maltoside, whose phenyl group does not interact so much with the subsite of the enzyme.

The feedback effects of sex steroid hormones on pituitary gonadotropin release in Turner's syndrome and Klinefelter's syndrome.

The present study was designed to elucidate the feedback relationship between the release of pituitary gonadotropins and sex steroid hormones in Turner's syndrome and Klinefelter's syndrome. LH-RH stimulation test was employed to evaluate the effects of sex steroids on the release of gonadotropins. The release of gonadotropins in response to LH-RH as well as in baseline level was suppressed after the treatment with estrogen (mestranol 0.08 mg/day) for 10 days, followed by the treatment of the same period with estrogen (mestranol 0.08 mg/day) and progesterone (chlormadinone acetate 2.0 mg/day) in combination in both syndromes. The inhibitory effect of the combined treatment was greater than that of the treatment with estrogen alone. Administration of testosterone propionate (25 mg/day) for 3 days resulted in suppression of the release of both gonadotropins in baseline level and in response to LH-RH in both syndromes, but the suppressive effect appeared to be less complete as compared with that of estrogen or estrogen-progesterone. It was thus verified that the feedback interaction between the pituitary gonadotropin release and sex steroids such as estrogen, estrogen-progesterone or testosterone was operative in the same fashion in the patients with Turner's syndrome and Klinefelter's syndrome.