Light and sugars are fundamental elements of plant metabolism and play signaling roles in many processes. They are also critical factors determining the condition of plants cultured in vitro. The aim of this work was to investigate the simultaneous influence of irradiance and sugar content in the medium on the growth and photosynthetic apparatus condition of Arabidopsis thaliana in vitro. Plants were grown on media containing 1 or 3% of sucrose or glucose at three irradiances: 25, 100, and 250 lmol m-2 s-1 (weak, medium, and strong light). Media without sugar were used for control plants. Plant growth parameters were measured and the following physiological processes were investigated: photosynthesis, blue light-induced chloroplast relocations, and xanthophyll cycle activity. The expression of genes related to these processes was analyzed. The presence of sugar in the medium was found to be essential for the growth of Arabidopsis in vitro. Weak light significantly limited growth and the capacity to acclimate to changing light conditions. Strong light was a source of stress in some cases. Contrary to earlier reports, exogenous sugars showed a positive effect on photosynthesis. At higher concentration they acted as photoprotectants, overcoming the negative influence of strong light on photosynthesis and the xanthophyll cycle. The expression of all investigated genes was influenced by irradiance and sugar presence. In many cases differential effects of sugar type and concentration could be observed. The specific effects of some irradiance/sugar concentration combinations point to possible interactions between sugar-and light-induced signaling pathways.
Background-Autosomal recessive Stargardt's disease is a macular degeneration characterised by a juvenile onset and a rapidly progressive course resulting in an atrophic macular area typically surrounded by yeliowish retinal flecks. Method-The disease locus has previously been assigned to markers from chromosome 1p21-pl3 by genetic linkage analysis in eight multiplex Stargardt's disease families.Results-In an extended analysis, the assignment to chromosome lp was confirmed in the majority of the 21 families with Stargardt's disease who were studied. In addition, a series of recombinant chromosomes further narrowed the Stargardt's disease region to an approximately 3 cM interval between markers at D1S424 and DlS497. Conclusion-Multipoint linkage analysis most probably excludes this locus in three of these families suggesting non-allelic heterogeneity with at least one additional minor Stargardt's disease locus. (BrJ Ophthalmol 1996;80:745-749 Here, we report our results on the genetic linkage analysis in 21 Stargardt's disease families. We confirm linkage of the disease locus to chromosome lp21-p13 in the majority of our families. In addition, this study has identified a series of recombinant Stargardt's disease chromosomes which together refine the previous localisation of the disease gene to a small interval on chromosome lp between markers at D1S424 and D1S497. In three out of our 21 Stargardt's disease families we found evidence for non-allelic heterogeneity of this condition suggesting the occurrence of at least one additional minor Stargardt's disease locus. Patients and methods CLINICAL STUDIESForty four affected and 28 non-affected at risk individuals belonging to 21 Stargardt's disease families were recruited from the Eye Care Center Vancouver (Canada) and the Eye Clinic Tubingen (Germany) (Fig 1). At least one patient per family was seen by one of the authors (DW or AE), Dr W Macrae (Toronto) (family 15), or Dr CC Ewing (Saskatoon) (family 13). All families were of white origin except family 1 which originated from China. All affected family members were diagnosed with having typical features of Stargardt's disease including the following criteria: (1) the Weber, Sander, Kopp, Walker, Eckstein, Wissinger, Zrenner, Grimm initial presence of fundus flavimaculatus with yellow 'flecks' in the macular and paramacular areas when patients were seen at younger age; (2) a normal appearance of the optic disc, blood vessels, and peripheral retina; (3) the presence of the typical dark choroid on fluorescein angiography; (4) normal to subnormal electro-oculogram (EOG), normal electroretinogram (ERG) for rods and cones in early stages, and abnormal dark adapted amplitudes of the ERG recordings in advanced cases; (5) mottled pigmentation of the macula; and (6)
Auxin is involved in a wide spectrum of physiological processes in plants, including responses controlled by the blue light photoreceptors phototropins: phototropic bending and stomatal movement. However, the role of auxin in phototropin-mediated chloroplast movements has never been studied. To address this question we searched for potential interactions between auxin and the chloroplast movement signaling pathway using different experimental approaches and two model plants, Arabidopsis thaliana and Nicotiana tabacum. We observed that the disturbance of auxin homeostasis by shoot decapitation caused a decrease in chloroplast movement parameters, which could be rescued by exogenous auxin application. In several cases, the impairment of polar auxin transport, by chemical inhibitors or in auxin carrier mutants, had a similar negative effect on chloroplast movements. This inhibition was not correlated with changes in auxin levels. Chloroplast relocations were also affected by the antiauxin p-chlorophenoxyisobutyric acid and mutations in genes encoding some of the elements of the SCF(TIR1)-Aux/IAA auxin receptor complex. The observed changes in chloroplast movement parameters are not prominent, which points to a modulatory role of auxin in this process. Taken together, the obtained results suggest that auxin acts indirectly to regulate chloroplast movements, presumably by regulating gene expression via the SCF(TIR1)-Aux/IAA-ARF pathway. Auxin does not seem to be involved in controlling the expression of phototropins.
The GLABRA (GL1) gene, belonging to the transcription factor-encoding myb gene family, is responsible for trichome formation in Arabidopsis thaliana (L.) Heynh. The leaves and stems of glabra1 mutant plants are devoid of trichomes. Having an easily observable phenotype, the gl1 mutation was one of the first markers established for genetic mapping of Arabidopsis thaliana. Since then, the GL1 gene has been assigned roles in other processes, also related to leaf structure. In this study we present some previously undescribed effects of the gl1 mutation on dark-induced senescence. This process was induced by covering selected mature leaves of Columbia wild-type and gl1 Arabidopsis with black paper for 4 days, while the plants remained growing in a normal photoperiod. While no visible differences in the external symptoms of senescence could be observed in the darkened leaves, the expression of senescence-associated genes was significantly lower in gl1 plants as compared to the wild type. The darkening of leaves led to a decrease in photosynthetic activity and the expression of photosynthesis-associated genes, in comparison to the control leaves. This effect was much less pronounced in gl1 than in the wild type plants. Therefore, gl1 plants seem to be less susceptible to dark-induced aging, suggesting a possible role for the GL1 gene in controlling the onset and progress of senescence. This result is also of practical importance, since gl1 is the genetic background of many other mutants. It may therefore be advisable to revise some of the results obtained with such mutants in light of findings presented here.
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