鼠尾草属四种植物的核型分析

本文对4种鼠尾草属(Salvia)植物的核型进行了分析,得出4种染色体核型:Salvia miltiorrhiza染色体数为2n=14,其核型公式为2n=8m+2sm+4st;S.tesquicola染色体数为2n=14,其核型公式为2n=4m+4sm+4st+2T;S.azurea var.grandiflora染色体数为20,其核型公式为2n=4m+10sm+4st+2t; S.verticillata染色体数为60,其核型公式为2n=20m+28sm+12st.     

红原县引种早熟与晚熟猫尾草的核型分析

对红原县引种早熟与晚熟猫尾草(Phleum pratense L.)细胞染色体进行核型分析.研究表明,早熟猫尾草染色体数为2n=28,染色体的核型为K(2n)=2n=4x=28=22m+4sm(SAT)+2st(SAT),其中第5、11对染色体为近中部着丝粒染色体,第8对染色体为亚端部着丝粒染色体,其余各对染色体为中部着丝粒染色体,第8对染色体携带随体;晚熟猫尾草染色体数为2n=42,染色体的核型为K(2n)=2n=6x=42=2M+24m+14sm+2sm(SAT),其中第3、4、6、11、12、13、14、20对染色体为近中部着丝粒染色体,第18对染色体为正中部着丝粒染色体,第22号为B染色体,其余各对染色体为中部着丝粒染色体,第11对染色体携带随体.早熟与晚熟猫尾草都属2A核型.     

春兰(Cymbidium goeringii(Rchb.f)Rchb.f.)的核型研究

用改进的染色体标本制片技术 ,报道了春兰 (Cymbidium goeringii (Rchb .f)Rchb .f .)的染色体核型 .研究结果表明 ,春兰体细胞染色体数目 2n =4 0 ,染色体基数x =2 0 .中期染色体中等大小 ,相邻染色体间长度变化不明显 ,染色体相对长度系数组成 (I .R .L .) =2L 2 0M2 14M1 4S .核型公式为 2n =2x =4 0 =2 0m 14sm 4st 2t.主要由中部着丝粒染色体和近中部着丝粒染色体组成 ,未见随体结构 .属于Stebbins核型的 2B型 ,核型不对称系数为 6 4 .2 2 .作者从染色体水平支持春兰在系统演化上归属于较进化的特化种类     

兵豆的细胞学研究

对兵豆 (LensculinarisMedic)进行了细胞学研究 .结果表明 :兵豆的染色体基数为 7;核型公式为 2N=2X =14 =8m( 2SAT) 4sm 2st ;核型类型属 3A型 .     

山东6种植物的染色体研究

对山东6种植物进行了染色体研究．白英(Solanum lyratum Thunb．)染色体数目为2n=24。核型公式K(2n)=2x=24=20m 4sm,核型“1A”;葎草(Humulus scandens(Lour．)Merr．)染色体数目为2n=16,核型公式K(2n)=2x=16=8m 8sm,核型“2A”;白刺花(Sophora vicifoliaHance．)染色体数目为2n=18。核型公式K(2n)=2x=18=2M 14m 2sm,核型“1A”;有斑百合(Lilium concolor var ．pulchellum(Fisch．)Regd．)染色体数目为2n=24,核型公式K(2n)=2x=24=4m 2sm 6st 12t,核型“3A”;野韭(Allium ramosum L.)染色体数目为2n=16 1B,核型公式K(2n)=2x=16=12m 2sm 2st 1B,核型“2A”;狼尾花(Lysimachia barystachys Bge．)染色体数目为2n=24,核型公式K(2n)=2x=24=14m 10sm,核型“2A”。     

皖西天堂寨三种黄精属植物的核型研究

首次报道了皖西天堂寨三种黄精属(Polygonatum)植物的染色体数目和核型,结果如下:湖北黄精(P. zanlanscianense) 核型为20n=2x=28=10m 8sm 10st,染色体长度比值3.49,属于3B核型;多花黄精(P. cyrtonema)核型为 2n=2x=22=2m 18sm 4st, 染色体长度比值2.38,属于3B核型;玉竹(P. odoratum)核型为2n=2x=18=8m 10sm(3sc), 染色体长度比值2.84, 属于2B核型.分别与产自其它地区的同种植物的染色体数目和核型差异明显.     

粗柄独尾草染色体核型分析

对粗柄独尾草(Eremurus inderiensis (M.B.)Rgl.)体细胞染色体计数及其核型进行分析。结果表明：粗柄独尾草的染色体数目为2n=14；核型公式为2n=2x=14=10sm 4st，其核型类型其为3B。     

罗汉果与三种苦瓜属植物的核型比较分析

以罗汉果、苦瓜、木鳖子、云南木鳖种子根尖为实验材料,采用去壁低渗法进行染色体制片和核型分 析,为罗汉果的分类归属及品种选育、倍性育种提供细胞遗传学资料. 结果表明:罗汉果染色体28条,为二倍体, 基数为14,核型公式为2n=2x=28=10m+6sm+6st+2t+4T,核型类型为3A型;苦瓜染色体22条,为二倍体,基数为 11,核型公式为2n=2x=22=2M+20m,核型类型为1A型;木鳖子染色体28条,基数为14,核型公式为2n=2x=28= 2m+22sm(2SAT)+4st,核型类型为3A型;云南木鳖染色体24条,基数为12,核型公式为2n=2x=24=22m+2sm,核 型类型为1A型染色体数目和核型类型表明罗汉果和木鳖子的亲缘关系比较近,在分类系统上比较进化;苦瓜和 云南木鳖亲缘关系比较近,在分类系统上比较原始.核不对称系数也表明木鳖子和罗汉果在分类系统上比较进 化,苦瓜和云南木鳖比较原始.     

青藏高原东缘风毛菊属中两种植物的核型报道

利用压片法研究青藏高原东缘两种风毛菊属(Saussurea DC.)植物的染色体数目和核型,结果表明,紫苞雪莲(S.iodostegia)和抱茎风毛菊(S.chingiana)的染色体数目和核型分别为2n=2x=32=18m+14sm,2n=2x=28=24m+2sm+2st.根据Stebbins提出的核型分类原则,这2个种的核型都为2A型.2个种的染色体中均未发现随体.     

荚迷属两个种的核型研究

报道忍冬科 (Caprifoliaceae)荚迷属 (Viburnum) 2种植物的核型 ,臭荚迷 (V .foetidumWall.)为 2n =18,核型公式为 2n =2x =18=14m 4sm ,核型属于“2B”型 ;水红木 (V .cylindriumBuch .-HamexD .Don)为2n =18,核型公式为 2n =2x =18=12m 6sm ,核型亦属“2B”型 .这 2个种的染色体数目与文献报道一致 ,而其核型为首次报道 .     

Correlation between immunoglobulin light chain expression and variant translocation in Burkitt's lymphoma

Burkitt's-type lymphomas-leukaemias (BL) are monoclonal proliferations of malignant B lymphocytes. Irrespective of whether they carry the Epstein-Barr virus (EBV) genome, these tumour cells have been shown consistently to have one of the specific reciprocal chromosome translocations, t(8; 14), t(2; 8) or t(8; 22), involving the long arm of chromosome 8 (on 8q24) and chromosome 14, 2 or 22 (on 14q32, 2p12 and 22q11, respectively). The latter chromosomes have been shown recently to carry genes for immunoglobulin (Ig) heavy chains, and kappa and lambda light chains, respectively. Furthermore, the localization of kappa light chains within 2pcen-2p13 encompasses the breakpoint observed in Burkitt's translocation (2p12). It was therefore considered of interest to determine whether the expression of immunoglobulin chains in BL cells is related to the type of chromosomal anomalies observed. We report here that there is a direct relationship between expression of immunoglobulin light chains and specific type of translocation: BL cells with t(8; 22) express lambda chains, whereas those with t(2; 8) express kappa chains.     

The t(8; 14) chromosomal translocation occurring in B-cell malignancies results from mistakes in V-D-J joining

The reciprocal chromosome translocation, t(8;14), involving the heavy chain locus on chromosome 14 and the c-myc oncogene on chromosome 8 is a characteristic of the B-cell malignancies Burkitt's lymphoma and acute lymphoblastic leukaemia (ALL). We have cloned and sequenced the t(8; 14) breakpoints of an African Burkitt's lymphoma cell line, P3HR-1, and a pre-B cell ALL cell line, 380. In each case the region of chromosome 8 involved has recombined with a JH region on chromosome 14. The two sites of breakage on chromosome 8 lie within 70 base pairs (bp) of one another. At each joining site, sequences homologous to the signal sequences thought to be recognized by the V-D-J recombinase were identified, as were N regions. In B-cell chronic lymphocytic leukaemias (B-CLL) carrying the t(11; 14) chromosome translocation and in follicular lymphomas carrying the t(14; 18) translocation, the V-D-J recombinase is implicated in the mechanism of chromosomal translocations. We speculate that the same enzymatic mechanism is responsible for the t(8; 14) translocations in African Burkitt's lymphoma and pre-B cell ALL.     

Inversion of chromosome 14 marks human T-cell chronic lymphocytic leukaemia

Rare cases of chronic lymphocytic leukaemia (CLL) in man stem from the malignant proliferation of T cells. The disease is usually more aggressive clinically than B-cell-derived CLL. Various haematological tumours are associated with specific chromosome aberrations (for example, refs 1, 2). Only limited numbers of T-cell CLL patients have so far been studied cytogenetically and, whereas chromosome 12 seems particularly to be involved in B-cell CLL, several markers have been found in T-cell tumours. Recently, by stimulating malignant clones with different mitogens, novel chromosome abnormalities have been detected in T-cell CLL. Using the same approach for additional cases of T-cell CLL, we now report that the most consistent chromosome change is an inversion of the long arm of chromosome 14, inv(14)(q11 q32), in four of five patients. Another remarkable chromosome aberration is trisomy for the long arm of chromosome 8, found in three of five patients.     

Clustering of breakpoints on chromosome 11 in human B-cell neoplasms with the t(11;14) chromosome translocation

The t(11;14) (q13;q32) chromosome translocation has been reported in diffuse small and large cell lymphomas and in chronic lymphocytic leukaemia (B-CLL) and multiple myeloma. Because chromosome band 14q32 is involved in this translocation, as well as in the t(8;14) (q24;q32) translocation of the Burkitt tumour, interruption of the immunoglobulin heavy-chain locus was postulated for this rearrangement. We have cloned the chromosomal joinings between chromosomes 11 and 14 and also between chromosomes 14 and 18, in B-cell tumours carrying translocations involving these chromosomes, and suggested the existence of two translocated loci, bcl-1 and bcl-2, normally located on chromosomes 11 (band q13) and 18 (band q21) respectively, involved in the pathogenesis of human B-cell neoplasms. The results indicate that in the leukaemic cells from two different cases of CLL, the breakpoints on chromosome 11 are within 8 nucleotides of each other and on chromosome 14 involve the J4-DNA segment. Because we detected a 7mer-9mer signal-like sequence with a 12-base-long spacer on the normal chromosome 11, close to the breakpoint, we speculate that the t(11;14) chromosome translocation in CLL may be sequence specific and may involve the recombination system for immunoglobulin gene segment (V-D-J) joining.     

Metallothionein gene cluster is split by chromosome 16 rearrangements in myelomonocytic leukaemia

The metallothioneins (MTs) are a family of proteins of low relative molecular mass which bind heavy-metal ions. MTs exist in several molecular forms (MT-I, MT-II) and are encoded by a multi-gene family containing at least 14 closely related genes and pseudogenes. These proteins function in the regulation of trace-metal metabolism, the storage of these ions in the liver, and as a protective mechanism against heavy-metal toxicity. Somatic cell hybridization has shown that most MT genes, including the functional MT genes (MT1A, MT1B, MT2A), lie on human chromosome 16. Using in situ hybridization, we have now localized the MT genes to band q22 of chromosome 16. This chromosomal band is also a breakpoint in two specific rearrangements, the inv(16)(p13q22) and t(16; 16)(p13;q22) rearrangements, found in a subgroup of patients with acute myelomonocytic leukaemia (AMML). Hybridization of a MT probe to malignant cells from two patients with an inv(16) showed labelled sites on both arms of the inverted chromosome, indicating that the breakpoint at 16q22 splits the MT gene cluster. Similar results were obtained when this probe was hybridized to metaphase cells from two patients with a t(16; 16). These results suggest that the MT genes or their regulatory regions may function as an 'activating' sequence for an as yet unidentified cellular gene located at 16p13.     

Progression from lymphoid hyperplasia to high-grade malignant lymphoma in mice transgenic for the t(14; 18)

Follicular lymphoma, the most common human lymphoma, characteristically has a t(14; 18) interchromosomal translocation. It is typically an indolent disease comprised of small resting B cells, but frequently develops into a high-grade lymphoma. The t(14; 18) translocates the Bcl-2 gene, generating a deregulated Bcl-2-immunoglobulin fusion gene. Bcl-2 is a novel inner mitochondrial membrane protein that extends the survival of certain cells by blocking programmed cell death. To determine the oncogenic potential of the t(14; 18) translocation, we produced transgenic mice bearing a Bcl-2-immunoglobulin minigene that structurally mimicked the t(14; 18). An indolent follicular hyperplasia in these transgenic mice progressed to a malignant diffuse large-cell lymphoma. The long latency, progression from polyclonal to monoclonal disease, and histological conversion, are all suggestive of secondary changes. Half of the immunoblastic high-grade lymphomas had a rearranged c-myc gene. Our transgenic mice provide an animal model for tumour progression in t(14; 18) lymphoma and show that prolonged B-cell life increases tumour incidence.     

A chromosome 14 inversion in a T-cell lymphoma is caused by site-specific recombination between immunoglobulin and T-cell receptor loci

Specific chromosomal aberrations are associated with specific types of cancer (for review see ref. 1). The distinctiveness of each association has led to the belief that these chromosomal aberrations are clues to oncogenic events or to the state of differentiation in the malignant cell type. Malignancies of T lymphocytes demonstrate such an association characterized most frequently by structural translocations or inversions of chromosomes 7 and 14 (refs 7-9). Analyses of these chromosomally marked tumours at the molecular level may therefore provide insight into the aetiology of the cancers as well as the mechanisms by which chromosomes break and rejoin. Here we report such an analysis of the tumour cell line SUP-T1 derived from a patient with childhood T-cell lymphoma carrying an inversion of one chromosome 14 between bands q11.2 and q32.3, that is, inv(14) (q11.2; q32.2). These are the same chromosomal bands to which the T-cell receptor alpha-chain (14q11.2) and the immunoglobulin heavy-chain locus (14q32.3) have been assigned. Our analysis reveals that this morphological inversion of chromosome 14 was mediated by a site-specific recombination event between an immunoglobulin heavy-chain variable region (Ig VH) and a T-cell receptor (TCR) alpha-chain joining segment (TCR J alpha). S1 nuclease analysis shows that this hybrid gene is transcribed into poly(A)+ RNA.     

Translocation of the p53 gene in t(15;17) in acute promyelocytic leukaemia

Recent studies have demonstrated that the cellular tumour antigen p53 (ref. 1) can complement activated ras genes in the transformation of rat fibroblasts, suggesting that the gene encoding p53 may act as an oncogene. Here, by using in situ chromosomal hybridization, we have mapped the p53 gene to human chromosome 17, at bands 17q21-q22, the region containing one of the breakpoints in the translocation t(15;17) (q22;q21) associated with acute promyelocytic leukaemia (APL). Hybridization of p53 and erb-A (17q11-q12) probes to malignant cells from three APL patients indicated that the p53 gene is translocated to chromosome 15 (15q+), whereas erb-A remains on chromosome 17. Analysis of variant translocations demonstrates that the 15q+ chromosome contains the conserved junction, suggesting a role for p53 in the pathogenesis of APL. However, rearrangements of the p53 gene were not detected on Southern blotting of DNA from leukaemic cells of four APL patients with t(15;17).     

Isolation and polymorphic frequency detection of a novel STR on human chromosome 14q24.3

A single copy fragment (FD14-ca 1) cantaining 22 CA repetitive units was isolated with (CA)₁₅ oligonucleotide probe from a human chromosome 14q24.3 probe pool generated by microdissection, and proved to be a new short tandem repeat (STR) sequence through querying in GenBank of NCBI. The STR has 11 alleles in Chinese. and its polymorphic information content (PIC) is 0.85. Mendelian segregation was shown in 2 Chinese pedigrees with two generations; This STR has been accurately relocalized on chromosome 14q24.3 by fluorescencein situ hybridization (FISH). The accession numbers of this STR in GDB and Gnknk database are D14S1435 and G31413 respectively. This STR would be able to be regarded as a novel genetic marker which can increase the genetic map accuracy in this chromosome region and improve the gene diagnosis on some genetic diseases located in chromosome 14q24.3 band.