Abscisic acid both promotes and inhibits photoperiodic flowering of Pharbitis nil

Abscisic acid (ABA) has been reported to have diverse effects on photoperiodic flowering. Activity of a natural ABA, (+)-( S )-abscisic acid (S-ABA), was recently suggested to be somewhat different from that of racemic ABA, which has been used in previous work. Use of S-ABA might enable clarification of the role of ABA in flowering. S-ABA inhibited flowering of the short-day plant Pharbitis nil (cv. Violet) when given before or 4 h after the start of a 14-h inductive dark period, and promoted flowering when given 12 h after the start of the dark period or later. The flower-promoting effect was observed when ABA was applied to the shoot apex. These results indicate that ABA has a dual effect on photoperiodic flowering of P. nil : it may inhibit the time-measuring process as well as promote some processes that proceed after generation of the flowering stimulus.     

Flowering response of Ipomoea batatas scions grafted onto Pharbitis nil stocks

Young seedlings of Ipomoea batatas (L.) Lam. cv. Big One did not form floral buds, but were induced to flower when grafted onto Pharbitis nil Chois. cv. Violet with its cotyledons exposed to a 16 h dark period (SD). Four SD were required to induce flowering in I. batatas scions when the grafted plants were first grown under an 8 h dark period (LD) for 18 days and then exposed to SD. Transmission of the flowering stimulus across the graft union required 4 days. It was also slow in the graft combination of P. nil and P. nil , but increased greatly when the graft union was established more completely. These results suggest that the flowering stimulus of P. nil may move symplastically and its life may be between 4 and 6 days. Although the leaves of I. batatas inhibited flowering, the flowering response of P. nil grafted onto I. batatas suggested that the involvement of a transmissible flowering-inhibitor was unlikely.     

shk1-D, a dwarf Arabidopsis mutant caused by activation of the CYP72C1 gene, has altered brassinosteroid levels

Brassinosteroids (BRs) are plant steroidal hormones that regulate plant growth and development. An Arabidopsis dwarf mutant, shrink1-D (shk1-D), was isolated and the phenotype was shown to be caused by activation of the CYP72C1 gene. CYP72C1 is a member of the cytochrome P450 monooxygenase gene family similar to BAS1/CYP734A1 that regulates BR inactivation. shk1-D has short hypocotyls in both light and dark, and short petioles and siliques. The seeds are also shortened along the longitudinal axis indicating CYP72C1 controls cell elongation. The expression of CPD, TCH4 and BAS1 were altered in CYP72C1 overexpression transgenic lines and endogenous levels of castasterone, 6-deoxocastasterone and 6-deoxotyphasterol were also altered. Unlike BAS1/CYP734A1 the expression of CYP72C1 was not changed by application of exogenous brassinolide. We propose that CYP72C1 controls BR homeostasis by modulating the concentration of BRs.     

Simultaneous phenotyping of pig plasma α-protease inhibitors (PI1, PO1A, PO1B, PI2) and four other proteins (PO2, TF, CP, HPX) by a simple method of 2D horizontal electrophoresis

A simple and rapid method of 2D agarose gel (pH 5.4)-horizontal polyacrylamide gel (pH 9.0) electrophoresis was developed for the simultaneous phenotyping of pig plasma alpha-protease inhibitors (protease inhibitor-1 and -2; postalbumin-1A and -1B), postalbumin-2, transferrin, ceruloplasmin and haemopexin. These eight plasma proteins were clearly visible on gels stained with Coomassie Brilliant Blue G250. The 2D patterns and mobilities of several variants of alpha-protease inhibitors were described. By using two agarose gels and 10 polyacrylamide gels, 120 samples were easily analysed in a day. Since alpha-protease inhibitors show extensive polymorphism and as the gene for postalbumin-2 is closely linked to the halothane sensitivity locus Hal, this method is a useful tool for conducting parentage control and for predicting Hal genotypes of individual pigs.     

Induction of A:T to G:C transition mutations by 5-(2-chloroethyl)-2'-deoxyuridine (CEDU), an antiviral pyrimidine nucleoside analogue, in the bone marrow of Muta Mouse

5-(2-chloroethyl)-2'-deoxyuridine (CEDU) is a pyrimidine nucleoside analogue formerly in development for the treatment of herpes simplex virus infections. The compound proved clearly mutagenic in the mouse spot test and exhibited weak activity in the Salmonella reverse mutation test, which led to the termination of the compound's development. In another study, CEDU, administered orally to beta-galactosidase (lacZ) transgenic mice (Muta Mouse) for five days, induced a clear increase in lacZ mutant frequencies in spleen, lung, and bone marrow. In the present follow-up study, we analyzed 32 of those lacZ mutants isolated from the bone marrow of the Muta Mouse animals of the experiments mentioned above, in order to obtain further information on the type of mutations induced by CEDU. CEDU induced a pronounced increase in A:T to G:C transitions. The distribution of A:T to G:C transitions was clearly non-random, showing a bias towards T to C substitutions in the coding DNA strand and a preference to occur in the sequence motif 5'-(G or C)-T-G-3'. Our data support the hypothesis that CEDU, after being phosphorylated, is incorporated into cellular DNA in place of thymidine, which leads to mispairing with guanosine during subsequent DNA replication. As a result, the compound is thought to exert its mutagenicity by inducing mismatches leading to T to C transitions. Our findings point towards a mode of mutagenic action of CEDU that differs fundamentally from that of other antiviral antinucleosides whose clastogenic and recombinogenic activities prevail.