ALBERT

Notes: Zusammenfassung Unter den 189 bisher genauer untersuchten spontan aufgetretenen Plastidenmutanten wurden bei 7,4% der gescheckten Pflanzen Abweichungen von einer zufallsgemäßen Plastidenentmischung gefunden. 1. An dieser Stelle werden Plastidenmutationen geschildert, bei denen die abgeänderten Plastiden während der Zellteilung einseitig in Tochterzellen bestimmter Lage gelangen. Diese Plastidenschecken sind an einer besonders schnellen Entmischung, an einer verringerten Zahl der Scheckungsflecken und an einer einseitigen Anordnung der wenigen Flecken zu erkennen. An einer Pflanze mit weißen Spitzenflecken ließ sich feststellen, daß die farblosen Plastiden während der Zellteilung bevorzugt in die spitzen wärts gelegenen Tochterzellen gelangten. 2. Bei einer der Pflanzen mit einseitiger Plastidenverteilung fehlten die bei einer Plastidenentmischung zu erwartenden “heteroplastomatischen Mischzellen”. In sehr jungen Blattstadien ließen sich die theoretisch zu fordernden Mischzellen noch nachweisen, und es ließ sich feststellen, daß in diesen Mischzellen die mutierten Plastiden unter Mithilfe der normalen Plastiden zu ergrünen vermochten. In homoplastomatisch mutierten Zellen vermochten die mutierten Plastiden unter bestimmten Bedingungen zwar Stärke zu kondensieren, aber kein Chlorophyll zu bilden. Das Scheckungsmuster dieser Pflanze ist dadurch gekennzeichnet, daß aus grün erscheinenden Zelldeszendenzen immer wieder weiße Zellen abgegeben werden. Bei Pflanze, denen Mischzellen fehlen, weil grüne Plastiden in die Degeneration der mutierten Plastiden hineingezogen werden, liegen umgekehrt grüne Zellinseln inmitten weißer Zelldeszendenzen. Die Beobachtungen zeigen, daß die Untersuchung der Scheckungsmuster wertvolle Hinweise auf das Verhalten plasmatischer Erbträger geben kann.

Notes: Summary Besides numerous cytoplasmic and plastid alterations, caused by a nuclear mutant of Epilobium, there was also induced a periclinal chimera which exhibited a poorly growing, dark green cytoplasmic alteration in the hypodermal palisade layer lying above the central tissue of a plastid alteration which is without chlorophyll. The cells of the colourless cell descendants shove into the gaps of the green palisade layer and form white “tissue windows”. They adapt themselves totally to the typical structure of the palisade layer.

Notes: Summary Seeds ofEpilobium hirsutum were treated with 0.5 mC35S isotope. One treated plant gave rise to variegated plants when selfed. Crosses revealed that this was caused by a recessive gene mp2 which induces plastid mutations. That the observed variegation was due to mutations of the plastids could be derived from the evidence of the characteristic patterns of the leaves and from the occurrence of actual mixed cells. Maternal inheritance of the mutated plastids could not be demonstrated as the mp2 gene induces most of the plastid mutations too late in the development of the leaves to exert an effect on the shoots and cell lines giving rise to egg cells.

Notes: Summary The cross experiments on cytoplasmic inheritance in Epilobium reveal the important fact that the cytoplasm of the cells contains numerous constituents (viz. plastied etc.), which can segregate intraindividually. The mutated plastids have to be investigated immediately after the mutation and not after an indefinite time of intraindividual segregation. Unfortunately, the rate of plastid mutation is too low to be observed microscopically. It is known that the rate of plastid mutability can be increased by the influence of certain nuclear genes. Such gene mutations increasing the plastid mutability, also in Epilobium, were looked for in mutation experiments with radioactive isotopes. In the experiments (Table 1) 3 genes inducing plastid mutations more frequently were detected among 849 induced nuclear gene mutations. One of these 3 genes, the mp 1-gene, is described in this publication. In nearly 100% of the homozygote, recessive (mp 1 mp 1) conditions the mp 1 gene induces numerous various plastome and plasmone mutations. The spectrum of these induced mutations is different from the spectrum of spontaneous mutations (Table 3). It seems possible, that the plastid mutations were indirectly induced by plasmone alterations which are formed presumablely in mp 1 mp 1 plants. 1–4% plastid-mutations are induced by the plasmone of the former mp 1 mp 1-plants, even after the elimination of the mp 1 mp 1-genes. The spontaneous mutation rate is only 0,2%. The induced plastid and plasmone-mutations could be analysed by the backcrossing between mp 1 mp 1 ♀xhirsutum Essen Mp 1 mp 1 ♂. In this crossing the few mutated constitutents present in the eggcells were transfered by maternal inheritance to the F1, whereas the effect of the mp 1-gene was inactivated in the heterozygote condition. The plastid mutations were inherited maternally (Table 7). They are characterized by real mixed cells with two genetically different plastids in young state of cell-differentiation (Table 5) and also by an alternative spotting in specific “verschachtelt” patterns. The properties of plastids can be changed by mutation variably. The pigment content of the altered tissue can vary from white, cream, yellow over different degrees to green resp. and is determined by a specific alteration or a specific degree of degeneration. The behaviour of the plastids during their distribution at the cell division can vary from a distribution by chance to an onesided distribution. This onesided distribution can be recognized by a onesided situation of the spots and by an acceleration of the outsorting of plastids. The physiological behaviour of the plastids can be altered by the interaction of plastids within the plastome. Mixed cells can disappear in aged cells both the ways mutually influencing the different plastids. Anatomical disturbance within leaf development can arise by alterations of the frequency of cell divisions. Even the greenness of plastids can be increased by environment in certain plastotypes. Numerous backmutations (=restitutions) were induced by the mp 1-gene in the yellowish cells with colourless plastids at 2 specific plastotypes, and a specific variegation pattern is produced in this way. But in most plasmotypes such an influence of the mp 1-gene could not be observed. The viability of the white seedlings of the crossings on white branches of the variegated plants can vary. Plastotypes with anatomical disturbances do not produce seeds (Table 6). A plastotype with very small, white spots containing in average 71% green tissue failing to outsort pure white shoots and also of green progenies in spite of the variegated leaves was thought to be a combination with the “rhytidiophyllum”-plasmotype. The hypothesis is: that the green “rhytidiophyllum”-seedlings are not viable and that this plasmotype induces plastome-alterations in so late state of development that the cell divisions in the leaves are not sufficient for a complete outsorting in poor white shoots. Some plastotypes were periclinal chimeras with plasmotypes. The progenies of 2 further alterations were uniformly yellow-green. Plasmone alterations can be supposed to be by the failure of variegation. Disturbances of shoot or leaf-development are frequently observed at the plasmone alterations arising in combination with plastid mutations. They are similar but not identical with the plasmone alterations of the Epilobium hirsutum EssenxEpilobium parviflorum Tübingen hybrid. Plasmone alterations are characterized by sudden arising or by quantitative changes of the disturbances and also by the failure of mixed cells with different plastotypes and by gliding alterations of the patterns. Such behaviour can be explained by a flowing or onesided alteration of the ratios between the hereditable units, which occur in the cells in higher numbers. Alterations similar to the alteration “stenophyllum” (Fig. 13) of the Epilobium hirsutum EssenxEpilobium parviflorum Tübingen do not flower, exceptionally after normalisation of the shoots. Alterations similar to “rhytidiophyllum” (Fig. 14) show an ill formation of seeds and a quantitative variegation in the formation of their small leaves. Each difference between two single shoots was inherited maternally to the progenies. Alterations similar to “irregulare” (Fig. 16) show defects in the formation of the plumule of seedlings. All these differences were inherited maternally over at least 3 generations, even of flower-reciprocal crossing of the various alterations with one another (Table 10).