scholarly journals Correlation between Expression of mcy Gene Cluster Relevant to Microcystin Production and Cell Cycle of Microcystis viridis

2008 ◽  
Vol 44 (4) ◽  
pp. 195-202
Author(s):  
MOTOO UTSUMI ◽  
KEISHI KAMEYAMA ◽  
KUNIHIRO OKANO ◽  
NORIO SUGIURA

2004 ◽  
Vol 19 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Keishi Kameyama ◽  
Norio Sugiura ◽  
Yuhei Inamori ◽  
Takaaki Maekawa


Author(s):  
H. Fryssira ◽  
P. Makrythanasis ◽  
A. Kattamis ◽  
K. Stokidis ◽  
B. Menten ◽  
...  


1994 ◽  
Vol 14 (5) ◽  
pp. 2936-2945
Author(s):  
B M Moats-Staats ◽  
H W Jarvis ◽  
A J D'Ercole ◽  
A D Stiles

During the course of antisense oligodeoxynucleotide (oligo) inhibition experiments investigating the role of insulin-like growth factor I (IGF-I) in the WI-38 cell cycle, we found that a sense-strand oligo (S oligo), used as a control, inhibited DNA synthesis 90 to 95%. S1 nuclease protection assays demonstrated that this S oligo formed intracellular duplexes with WI-38 RNA, and Northern (RNA) hybridization analyses demonstrated specific hybridization of this 32P-labeled S oligo to 1.8-, 2.3-, and 3.2-kb RNAs. We have cloned and sequenced a 2,251-bp cDNA, designated BB1, corresponding to the 2.3-kb RNA. Decoding of the BB1 cDNA sequence reveals several open reading frames arranged in a motif similar to that seen in proteins subject to translational control mechanisms. Homology searches of nucleic acid and protein data bases reveal no significant homology of BB1 with known sequences other than a 234-bp region in the BB1 5' untranslated region that shared 97% homology with a region in the 3' untranslated region of the human cdc42 mRNA. S1 nuclease protection analyses performed with IGF-I gene fragments and computer homology searches demonstrated that the BB1 RNA does not derive from transcription from the opposite strand of the IGF-I gene. Northern hybridization analyses of RNA extracted from serum-starved HeLa S3 cells demonstrated that steady-state BB1 RNA levels increased upon serum growth stimulation, with steady-state levels peaking 4 h after release from the block induced by serum starvation. Antisense oligo inhibition experiments using specific BB1 antisense oligos targeted to the putative open reading frames of the BB1 RNA reduce DNA synthesis of HeLa S3 cells to 15% of control levels, indicating that the BB1 RNA is essential for cell cycle traversal and, as such, encodes a growth-reguLating gene product.



1994 ◽  
Vol 14 (5) ◽  
pp. 2936-2945 ◽  
Author(s):  
B M Moats-Staats ◽  
H W Jarvis ◽  
A J D'Ercole ◽  
A D Stiles

During the course of antisense oligodeoxynucleotide (oligo) inhibition experiments investigating the role of insulin-like growth factor I (IGF-I) in the WI-38 cell cycle, we found that a sense-strand oligo (S oligo), used as a control, inhibited DNA synthesis 90 to 95%. S1 nuclease protection assays demonstrated that this S oligo formed intracellular duplexes with WI-38 RNA, and Northern (RNA) hybridization analyses demonstrated specific hybridization of this 32P-labeled S oligo to 1.8-, 2.3-, and 3.2-kb RNAs. We have cloned and sequenced a 2,251-bp cDNA, designated BB1, corresponding to the 2.3-kb RNA. Decoding of the BB1 cDNA sequence reveals several open reading frames arranged in a motif similar to that seen in proteins subject to translational control mechanisms. Homology searches of nucleic acid and protein data bases reveal no significant homology of BB1 with known sequences other than a 234-bp region in the BB1 5' untranslated region that shared 97% homology with a region in the 3' untranslated region of the human cdc42 mRNA. S1 nuclease protection analyses performed with IGF-I gene fragments and computer homology searches demonstrated that the BB1 RNA does not derive from transcription from the opposite strand of the IGF-I gene. Northern hybridization analyses of RNA extracted from serum-starved HeLa S3 cells demonstrated that steady-state BB1 RNA levels increased upon serum growth stimulation, with steady-state levels peaking 4 h after release from the block induced by serum starvation. Antisense oligo inhibition experiments using specific BB1 antisense oligos targeted to the putative open reading frames of the BB1 RNA reduce DNA synthesis of HeLa S3 cells to 15% of control levels, indicating that the BB1 RNA is essential for cell cycle traversal and, as such, encodes a growth-reguLating gene product.





2001 ◽  
Vol 7 (5) ◽  
pp. 349-358 ◽  
Author(s):  
N. Misawa ◽  
K. Kawashima ◽  
F. Kondo ◽  
B.M. Allos ◽  
M.J. Blaser


2004 ◽  
Vol 70 (11) ◽  
pp. 6370-6378 ◽  
Author(s):  
Leanne A. Pearson ◽  
Michael Hisbergues ◽  
Thomas B�rner ◽  
Elke Dittmann ◽  
Brett A. Neilan

ABSTRACT The cyanobacterium Microcystis aeruginosa is widely known for its production of the potent hepatotoxin microcystin. Microcystin is synthesized nonribosomally by the thiotemplate function of a large, modular enzyme complex encoded within the 55-kb microcystin synthetase (mcy) gene cluster. Also encoded within the mcy gene cluster is a putative ATP binding cassette (ABC) transporter, McyH. This study details the bioinformatic and mutational analyses of McyH and offers functional predictions for the hypothetical protein. The transporter is putatively comprised of two homodimers, each with an N-terminal hydrophobic domain and a C-terminal ATPase. Phylogenetically, McyH was found to cluster with members of the ABC-A1 subgroup of ABC ATPases, suggesting an export function for the protein. Two mcyH null mutant (ΔmcyH) strains were constructed by partial deletion of the mcyH gene. Microcystin production was completely absent in these strains. While the mcyH deletion had no apparent effect on the transcription of other mcy genes, the complete microcystin biosynthesis enzyme complex could not be detected in ΔmcyH mutant strains. Finally, expression levels of McyH in the wild type and in ΔmcyA, ΔmcyB, and ΔmcyH mutants were investigated by using immunoblotting with an anti-McyH antibody. Expression of McyH was found to be reduced in ΔmcyA and ΔmcyB mutants and completely absent in the ΔmcyH mutant. By virtue of its association with the mcy gene cluster and the bioinformatic and experimental data presented in this study, we predict that McyH functions as a microcystin exporter and is, in addition, intimately associated with the microcystin biosynthesis pathway.





2009 ◽  
Vol 2 (3) ◽  
pp. 119-128 ◽  
Author(s):  
Eva Lattka ◽  
Thomas Illig ◽  
Joachim Heinrich ◽  
Berthold Koletzko


Genome ◽  
1989 ◽  
Vol 32 (3) ◽  
pp. 365-372 ◽  
Author(s):  
T. Starr ◽  
A. M. Howell ◽  
J. McDowall ◽  
K. Peters ◽  
A. M. Rose

We have isolated probes for DNA polymorphisms across the linkage group I gene cluster in Caenorhabditis elegans, using Tc1-linkage selection. The probes detect strain polymorphism between the wild-type strains of var. Bristol and var. Bergerac. As a result of mapping the sites hP4, hP5, hP6, hP7, hP9, and sP1, more than 1000 kilobases (kb) of cloned cosmid DNA has been positioned on the genetic map. We found there is more DNA per map unit in the center of the gene cluster than expected on the basis of the genomic average. Furthermore, the amount is not constant across the entire region but reaches a peak in the hP9 unc-13 interval. To find the coding regions, we examined DNA cross-homology between two species, Caenorhabditis elegans and Caenorhabditis briggsae. Approximately one-third of the DNA in the hP5 hP9 interval was examined for coding regions and 21 sequences were identified within 318 kb of DNA.Key words: Caenorhabditis elegans, physical map, DNA polymorphisms, genetic mapping, Caenorhabditis briggsae.



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