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Several Arabidopsis mutants of the ecotype Dijon were isolated that show resistance to the herbicide acifluorfen, which inactivates protoporphyrinogen oxidase (PPOX), an enzyme of tetrapyrrole biosynthesis. This enzyme provides protoporphyrin for both Mg chelatase and ferrochelatase at the branchpoint, which leads to chlorophyll and heme, respectively. One of the mutations, aci5-3, displays semidominant inheritance. Heterozygous progeny showed yellow-green leaves, while the homozygous seedlings were white and inviable, but could be rescued by supplementing the medium with sugar. Interestingly, the expression of neither of the two forms of PPOX was altered in the mutant, but the rate of synthesis of 5-aminolevulinate, the precursor of all tetrapyrroles, was drastically reduced. Genetic mapping revealed the mutant locus is closely linked to the ch42 marker, which is itself located in the CHLI-1 gene which codes for one of the three subunits of Mg chelatase. The cs mutant also shows a defect in this gene, and test for allelism with aci5-3 confirmed that the two mutations are allelic. Sequencing of the wild type and aci5-3 alleles of CHLI-1 revealed a single base change (G718A), which results in a D240N substitution in the CHLI-1 protein. In the homozygous aci5-3 mutant no CHLI-1 RNA or protein could be detected. Strikingly, CHLH and CHLI-2 transcripts were also absent. This indicates the existence of a feedback-regulatory mechanism that inactivates the genes encoding certain Mg chelatase subunits. The basis for the semidominant inheritance pattern and the relationship between herbicide resistance and modified gene expression is discussed.

One of the key regulatory enzymes of the chlorophyll biosynthesis pathway is magnesium (Mg) chelatase, consisting of three different subunits CHLI, CHLD and CHLH. While CHLH and CHLD are encoded by a single gene each in Arabidopsis, CHLI is encoded by two homologous genes, ChlI 1 and ChlI 2. Analysis of the acifluorfen herbicide resistant mutant aci5 revealed an alteration of the ChlI 1 gene. This mutant as well as wild type plants contained similar transcript levels of the ChlI 1 and ChlI 2 genes. Moreover, the transcripts of both alleles of the ChlI 1 gene were present in the cs (ch42-2)/aci5 hybrid which showed an albina phenotype. Comparison of the amino acid sequence of CHLI 1 and CHLI 2 encoded in the genome of aci5 and wild type revealed in particular alterations of the C-terminal end which are suggested to be responsible for the decreased ability of CHLI 2 to participate in the formation of the CHLI ring-like structure of the Mg chelatase complex.

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The research into the genetic control of flower formation is a rapidly evolving field of plant developmental biology. An ABC model of the genetic control of floral morphogenesis based on the studies of Arabidopsis thaliana mutants [1] envisaged the flower structure as a pattern comprising four organ whorls, with the particular organ development in each whorl specified by the combined activities of several genes. The expression of the A class genes APETALA1 ( AP1 ) and APETALA2 ( AP2 ) determines for the development of sepals (whorl 1). The development of carpels (whorl 4) is specified by the C class gene AGAMOUS ( AG ). The combined activities of the A and C genes together with the B genes APETALA3 ( AP 3 ) and PISTILLATA ( PI ) specify the development of petals and stamens (whorls 2 and 3, respectively). The ABC model postulates that the mutations in these genes would change the organ specificity in particular whorls. In several ABC mutants, the number of flower organs is changed; therefore a hypothesis was put forward that these genes specify both the identity of flower organs and flower organ initiation [2]. However, the mechanism of such specification is poorly understood. When working out the mathematical model of floral development based on the ABC-model postulates, we found that the existing evidence on the functions of the ABC genes did not sufficiently clarify the nature of changes in the arrangement of flower organs in the mutants. It follows that the processes that determine spatial pattern formation in the flower must be studied in more detail [3].There are two hypotheses describing the process of spatial pattern formation in the developing flower. The first one presumes that floral development proceeds acropetally, from periphery towards the center [4]. The development of each whorl is triggered by a signal from the whorl on the outside. The second hypothesis maintains that in floral development, the formation of organ spatial pattern precedes the initiation of corresponding organs [5]. Recently Chub and Penin [6] suggested that the spatial patterning may advance both acropetally and basipetally.The present study aimed at elucidating, by mathematic modeling, the basic aspects of spatial flower patterning in order to recognize the effects of the ABC genes on flower organ arrangement. The modeling demonstrated that organ spatial pattern formation in flowers was regularly scheduled and advanced in two directions, acropetally in the perianth and basipetally in the stamens and carpels. We demonstrated that AP2 (class A) and AG (class C) both specified the particular flower organs and also determined the acropetal and basipetal patterning zones in the floral meristem (APZ and BPZ, respectively).The structure of the mathematic model for specifying the arrangement of flower organs. To ascertain the timetable of organ arrangement, we developed a mathematical model taking into consideration the inhibitory impact theory [7], which postulates that the shoot apex and leaf initials excrete a substance that inhibit...