巻号一覧
41 巻, 6 号
選択された号の論文の4件中1～4を表示しています
- |<
- <
- 1
- >
- >|
-
KOICHIRO TSUNEWAKI1966 年 41 巻 6 号 p. 413-426
発行日: 1966年
公開日: 2007/05/21
ジャーナル フリーBased on three facts, i.e., (1) three common wheats, Prelude, Jones Fife and Macha form a necrosis triangle, (2) a 27:37 segregation ratio of necrotic vs. normal plants was obtained in the F2 generation of the cross, Chinese Spring x Macha, and (3) three genes, Ne1, Ne2 and Ne3, were located in different chromosomes, Tsunewaki and Kihara (1962) proposed a three gene hypothesis for necrosis, for whose appearance the genes Ne1, Ne2 and Ne3 were assumed to be necessary.
In order to work out further proofs for this hypothesis, two experiments were carried out. In the first experiment, Macha was crossed to Chinese Spring monosomics and the phenotypes of the F1 plants in relation to their chromosome numbers were studied. In the second experiment, F2, F3 and some F4 hybrids of the cross, Chinese Spring mono-3D x Macha, were studied by test-crossing them to Prelude, Jones Fife and Macha.
Against the expectation, the following results were obtained, that disproved the three gene hypothesis;
(1) Chinese Spring carries a single complementary gene, Ch2, for chlorosis on chromosome 3D (formerly XVI).
(2) Macha carries a necrosis gene, Ne1, and a chlorosis gene, Ch1. However, it does not possess the other necrosis gene, Ne2.
From these results, it was concluded that necrosis (formerly, the epidemic type of necrosis) and chlorosis (formerly, its systemic type) are under control of two independent gene systems, each consisting of two complementary genes; necrosis is determined by Ne1 and Ne2, and chlorosis by Ch1 and Ch2 (formerly Ne3).
Genic as well as phenotypic relationship between the formerly proposed and the present system is diagrammed in Fig. 2. Furthermore, a single-gene and two-gene tester series were compared in relation to their efficiency for differentiating the nine possible genotypes for necrosis and chlorosis. It is concluded that the two-gene tester series is, at present, more efficient than the one-gene series.抄録全体を表示PDF形式でダウンロード (2015K) -
HIDETOSHI KISHIKAWA1966 年 41 巻 6 号 p. 427-437
発行日: 1966年
公開日: 2007/05/21
ジャーナル フリーIn the triploid rye plant with four accessory chromosomes, the cytological investigation was made and the behaviour of accessory chromosomes was compared with one in the original diploids. The results are summarized as follows.
1. The chromosomes in the triploid showed a relatively higher degee of pairing at mataphase I, viz., the modal configuration was found in 4III+3II+3I+BIV, and 5III+2II+2I+BIV and 3III+4II+4I+BIV followed. The association of normal chromosomes may not be influenced by the presence of accessory chromosomes. At stages between anaphase I and tetrad formation, various abnormalities were observed. In almost all of the cells the lagging of the chromosomes and their abnormal distribution were seen at anaphase I and II, and tetrad and pentad with micronuclei were most frequently observed.
2. The metaphase I configurations of accessory chromosomes in the triploid were the same as one in the original diploids, but their frequencies differed. The frequency of multivalents, such as quadrivalent and trivalent, was lower than that in the diploid. This indicates that the association of accessory chromosomes may be reduced by the increase of normal chromosome complements.
3. In the disjunction of accessory chromosomes, various abnormalities, such as the laggards, the abnormal distribution and the occurrence of tetrad with micronuclei, in the triploid were more frequent than those in the diploids. This fact indicates that the disjunction of accessory chromosomes may be disturbed by the increase of normal chromosome complements.抄録全体を表示PDF形式でダウンロード (3140K) -
日本遺伝学会賞受賞講演吉田 俊秀1966 年 41 巻 6 号 p. 439-451
発行日: 1966年
公開日: 2007/05/21
ジャーナル フリーThe present paper deals with karyological studies of tumor cells, with special regard to the relationship between chromosomal alteration and tumor development.
(1) In my first karyological study of the Yoshida ascites rat sarcoma (Yosida 1948), I found that the ascites tumor was good material for chromosomal study of tumor cells. In the karyological studies carried out in 1949a and 1949b, the mitotic cells were classified into three types; namely, normal, aberrant and disintegration types. As a result of those studies the normally dividing cells were considered to play an important role in tumor development.
(2) Karyotypes in the stemline cells of many tumors in mice and rats deviate from those of normal somatic cells (Tables 1 and 2). The karyotype of stemline lineage, however, is not always stable, but is easily replaced by another cell type, when a more vigorous cell or cells occur in the cell population. Instances of replacement of stemline karyotype in Yoshida rat sarcoma, MY mouse sarcoma, mouse lymphocytic leukemia P388 and mouse hepatomas MH 134 and 129P are given in this paper. Change of stemline karyotypes is accerelated when the tumor encounters an unusual hostile condition. Remarkable change of stemline karyotype was observed in drug resistant P388 in vitro lines, which developed after treatment with 8-azaguanine and amethopterin. In mouse ascites leukemia L-1210, karyotypes in all five drug resistant sublines were also different from that of the sensitive line. From the above several investigations, it can be concluded that chromosome alteration is important and might be a causative process in creating more vigorons cell types.
(3) From the karyological studies in various stages of tumor development, it is assumed that normal somatic cells may be converted to tumor cells by following four development stages: (i) Normal development (ND) stage, (ii) Mutant producing (MP) stage, (iii) Mutant selection (MS) stage, and (iv) Tumor development (TD) stage. Among mutant cells, genes favoring acceleration of cell division may be accumulated and finally, the cells they develop into malignant cells having the character of autonomous multiplication (Fig. 7).
(4) Tumors produced by tumor virus had mainly normal diploid karyotype. For the induction of tumors by virus a different mechanism from that described above should be considered.抄録全体を表示PDF形式でダウンロード (4442K) -
日本遺伝学会賞講演小関 治男1966 年 41 巻 6 号 p. 453-458
発行日: 1966年
公開日: 2007/05/21
ジャーナル フリーPDF形式でダウンロード (820K)
- |<
- <
- 1
- >
- >|