The plastome mutator of Oenothera continues to function as originally described

Summary Recently, Lindenhahn et al. (1985) hypothesized that the plastome mutator (pm) system in Oenothera originated through contaiminating cross-pollination and that the variegation was an example of hybrid plastome-genome incompatibility. Their evidence was based on restriction pattern analyses of white sectors which showed wild-type plastome III patterns rather than the wild-type plastome I patterns of the green portions of their plants. Their hypothesis does not adequately account for the results which our laboratories have obtained independently; the pm-system of Oenothera continues to generate many new and different plastome mutations following the genetic parameters as published originally (Epp 1973). Our studies support mutator gene function. The restriction pattern of the chloroplast DNA of five newly isolated pm-induced variegation sectors are reported here to show a restriction pattern identical to the green wild-type plastids. The restriction pattern reported by Lindenhahn et al. (1985) for their white sector plastids is different than we would expect from a pm-induced plastome mutation. Their overall analysis did not utilize many of the salient features of the genetics of Oenothera and of the pm-system. The white sectors they observed are probably due to an accidental contamination by plastome III plastids. Suggestions are made for delineating experimentally plastome mutations and hybrid incompatibility. For future analyses, a comparative study of numerous pm-induced sectors is recommended, since the pm-system readily generates many different plastome mutations with independent origins. This comparison would greatly assist in the interpretation of restriction patterns.     

Large Drosophila germline piRNA clusters are evolutionarily labile and dispensable for transposon regulation

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Plastid genomes in a regenerating tobacco shoot derive from a small number of copies selected through a stochastic process

The plastid genome (ptDNA) of higher plants is highly polyploid, and the 1000-10 000 copies are compartmentalized with up to approximately 100 plastids per cell. The problem we address here is whether or not a newly arising genome can be established in a developing tobacco shoot, and be transmitted to the seed progeny. We tested this by generating two unequal ptDNA populations in a cultured tobacco cell. The parental tobacco plants in this study have an aurea (yellowish-golden) leaf color caused by the presence of a bar(au) gene in the ptDNA. In addition, the ptDNA carries an aadA gene flanked with the phiC31 phage site-specific recombinase (Int) attP/attB target sites. The genetically distinct ptDNA copies were obtained by Int, which either excised only the aadA marker gene (i.e. did not affect the aurea phenotype) or triggered the deletion of both the aadA and bar(au) transgenes, and thereby restored the green color. The ptDNA determining green plastids represented only a small fraction of the population and was not seen in a transient excision assay, and yet three out of the 53 regenerated shoots carried green plastids in all developmental layers. The remaining 49 Int-expressing plants had either exclusively aurea (24) or variegated (25) leaves with aurea and green sectors. The formation of homoplastomic green shoots with the minor green ptDNA in all developmental layers suggests that the ptDNA population in a regenerating shoot apical meristem derives from a small number of copies selected through a stochastic process.     

Structural and Functional Characteristics of the Mutant Plastids from Extranuclear Variegated Forms of Sunflower

The electron-microscopic analysis of extranuclear variegated forms of sunflower demonstrated that plastids from white leaf areas are practically devoid of inner membrane structures. The mutants and the initial (wild-type) green line were compared by the contents of chlorophyll (Chl), carotenoids, and 70S ribosomes and by the activity of Rubisco. A mutant Var10 line was used to demonstrate that the primary characteristic manifestations of Chl deficiency include the synchronous retardation of the synthesis of a specific Chl precursor, 5-aminolevulinate, a decrease in the Chl a/b ratio to the level below that in the wild type, and the reduction of photosystem (PS) I Chl luminance. The progress of photodestructive processes in the mutant aggravated the listed disturbances; as a result, PSII complexes and light-harvesting complexes gradually degraded. The manifestation of the trait of Chl-deficiency notably varied depending on plant growth conditions (primarily, temperature and illumination regimes). The dependence of this manifestation on light and temperature was observed only at the early stage of development of pigment-containing tissues. When plants terminated this stage under low irradiation, they did not become Chl-deficient, and when their leaves were subsequently transferred to the conditions promoting the maximum pigment anomaly, the destructive processes did not advance in the mutant tissue. The authors assume that the plastom mutations under study impair the control over the expression of the structural plastogenes that determine the synthesis of pigment and protein components of the photosynthetic apparatus, rather than directly damage to the primary structures of plastogenes.     

Constitutive heterochromatin in early embryogenesis of Drosophila melanogaster

Summary The formation of constitutive heterochromatin was studied during the embryonic development of Drosophila melanogaster, using the C-banding technique. During embryonic cleavage, C-banded material is not seen in mitotic chromosomes; the differentiation between euchromatin and heterochromatin only occurs at blastoderm. This event correlates with the establishment of position-effect variegation.     

The lamin Dm0 allele Ari3 acts as an enhancer of position effect variegation of the wm4 allele in Drosophila

The association of lamin and lamin binding proteins with peripheral heterochromatin suggests the possibility that lamins may influence gene expression by participating in the epigenetic regulation of chromatin stucture. To test this hypothesis we have examined the effect of a recently generated partial loss-of-function lamin Dm₀ allele Ari3 on PEV of the w ^m4 allele in the Drosophila eye. The Lam ^Ari3 allele is characterized by a truncation of the COOH-terminal domain and lacks the CaaX box that localizes lamin to the inner nuclear membrane. We show that the Lam ^Ari3 allele strongly increased silencing of w ^m4 expression, thus acting as an enhancer of PEV. These results indicate that lamins may be involved in regulating gene silencing and heterochromatic spreading at the w ^m4 locus and provide evidence that lamins may contribute to the regulation of higher-order chromatin organization.     

Presence of putative Cycas necrotic stunt virus RNAs in Japanese primrose (Primula sieboldii E. Morren)

The study screened the putative viral RNA sequences in the cDNA library of Japanese primrose, and conducted a molecular approach in determining its presence in selected Primula sieboldii accessions showing characteristic viral symptoms. Three putatively viral non-homologous sequence groups of RNA were identified; however, coding for different proteins representing a complete virus structure, it was determined to be singly originating from Cycas necrotic stunt virus (CNSV). Subsequently, sequence-specific primers were customised based from the non-homologous-sequence groups; however, amplification data showed no association between the presence of the putative viral RNA sequences and the identified characteristic virus symptoms. Despite this, amplification of the three non-homologous sequences is fully correlated. Thus, Japanese primrose was potentially identified as an alternate host of CNSV.