Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Single-step mutants were isolated from the murine metastatic MDAY-D2 cell line after selection in toxic concentrations of wheat-germ agglutinin. They were partially characterized by measuring their relative level of resistance to WGA, PHA, Con A, RIC, and LCA (Lec phenotype), and by comparing their karyotype and their ability to produce metastases upon transplantation into syngeneic DBA/2 mice. Based on their Lec phenotype, a total of 19 independent isolates were ranked into 10 distinct classes. Among them, two EMS-induced mutants were nontumorigenic (Lec II, Lec III), one nonmetastatic (Lec IV), and one spontaneous mutant (Lec I) failed to produce blood-borne metastases. Other spontaneous mutants belonging to Lec I, Lec II, and other classes were as metastatic as their parents. The Lec IV phenotype was found to segregate independently from metastatic potential in somatic hybrids. Metastatic ability was recovered in mutants expressing the Lec IV phenotype, after further selection for resistance to RIC. Our results strongly suggest that the loss or reduction of the invasive property of tumor cells is associated with only few Lecr1 phenotypes and, therefore, that a restricted number of cell surface glyconjugates are essential for this particular function.
Somat Cell Mol Genet 1984 Sep
PMID:Metastatic properties of distinct phenotypic classes of lectin-resistant mutants isolated from murine MDAY-D2 cell line. 659 45

Sex-linked behavioral mutants were induced in Drosophila melanogaster with ethyl methanesulfonate (EMS) and isolated by direct visual observation of abnormal phenotypes. The four behavioral phenotypes used were flight-reduction, hyperactivity, hypoactivity and stress-sensitivity, and are easily discernable in either single or small populations of mutant flies. In one screen, forty-two behavioral mutants were recovered from strains derived from 800 mutagen-treated X chromosomes In a second screen, 139 behavioral mutants were obtained from 2369 X chromosomes. The high rate at which behavioral mutants were recovered in the second screen, when compared to new visibles (28) and new temperature-sensitive lethals (124), suggests that the isolation of behavioral mutations on the autosomes of Drosophila and in the genomes of larger insects should be practical.
Mol Gen Genet 1980
PMID:Behavioral mutants of Drosophila melanogaster. III. Isolation and mapping of mutations by direct visual observations of behavioral phenotypes. 677 Feb 27

Purified RNA polymerase II (RNA nucleotidyl-transferase; EC 2.7.7.6) extracted from flies possessing lesions in the Ultrabithorax-like (Ubl) locus of Drosophila melanogaster has altered activity in vitro (Greenleaf et al. 1979, 1980; Coulter and Greenleaf 1982). This strongly suggests that the Ubl locus encodes a subunit of RNA polymerase II. Ethyl methanesulfonate was used to induce a temperature-sensitive mutation in this locus. Flies either homozygous or hemizygous for this new X-linked mutation (Ublts) display viability comparable to that of wild-type flies at 22 degrees C but are lethal at 29 degrees C. The temperature-sensitive period for Ublts flies is between gastrulation (6 h, 29 degrees C) and pupation (9-10 days, 22 degrees C). Zygotes shifted from 22 degrees C to 29 degrees C die at either the late embryonic or first larval instar stage while temperature shifts of second and third instar larvae result in the lethal phase occurring at the pupal stage. Most pupae shifted from 22 degrees C to 29 degrees C undergo metamorphosis and eclose as adults. Adults are viable if placed at 29 degrees C; however, all females and some males become sterile if maintained at this temperature. Somatic recombination was used to induce clones homozygous for a null allele of Ubl at different stages of development. Clones of this null allele appear to be cell lethal indicating that the Ubl+ gene product is required at all stages of development. The viability of Ublts pupae and adults at 29 degrees C may result from only a partial reduction in activity caused by the mutation at this nonpermissive temperature.
Mol Gen Genet 1982
PMID:Developmental genetics of a temperature-sensitive RNA polymerase II mutation in Drosophila melanogaster. 681 24

The mutation frequency of DNA polymerase mutants of phage T4 treated with ethyl methanesulfonate (EMS) then incubated in the presence and absence of caffeine was studied using an rII reversion system. The DNA polymerase mutation is shown to be antimutagenic for EMS induction of reversions which occur by a GC to AT transition. Caffeine acts as a comutagen for the induction by EMS of mutant phages and produces a significant increase in the frequency of reversions from rII to r+. Caffeine is slightly mutagenic for the phage strain carrying the wild type polymerase and inhibits the action of the 3' leads to 5' exonuclease function of T4 DNA polymerase as measured in vitro. These findings suggest that caffeine acts by directly influencing nucleotide selection or the editing function of the DNA polymerase.
Mol Gen Genet 1980
PMID:Caffeine as a comutagen for ethylmethanesulfonate in strains of phage T4. 693 94

This paper describes studies to determine the role of the umuC gene product in the process of alkylation induced mutagenesis. An active umuC gene is necessary for most MMS induced mutagenesis but it is not essential for EMS nor for MNNG induced mutagenesis in either normal or adapted cultures. In this respect the umuC mutation differs from lexA mutations which have a striking effect on MNNG induced mutagenesis (Schendel, et al., 1978). These findings have prompted a re-evaluation of these previously published data and the advancement of an hypothesis which explains the lexA effect without evoking a role for error-prone repair in the process of alkylation induced mutagenesis. It was also observed that exposure to MNNG is capable of generating a small amount of W-reactivation and W-mutagenesis capacity in a umuC strain which is totally blocked for UV induced reactivation. In light of this result a possible function for the umuC gene product is discussed.
Mol Gen Genet 1980
PMID:The role of umuC gene product in mutagenesis by simple alkylating agents. 699 71

A newly-isolated Escherichia coli mutant suffers only about 10% as many mutations as normal strains on exposure to nitrosoguanidine. The responsible mutation, inm-1, maps at approximately minute 79 in the current E. coli genetic map. The mutant is normal for overall growth, nitrosoguanidine lethality, spontaneous mutagenesis, ultraviolet light lethality and mutagenesis, ethyl methanesulfonate lethality and mutagenesis, and the adaptive repair induced by alkylating agents. The existence of this mutation proves that nitrosoguanidine mutagenesis is not merely the result of reactions between the chemical and DNA, but requires specific cellular function(s), and underscores the peculiarity of nitrosoguanidine as a mutagen.
Mol Gen Genet 1980
PMID:An Escherichia coli mutant refractory to nitrosoguanidine mutagenesis. 699 58

An approach based on the synchronization of CHO cells after a first cell cycle incorporating a relatively low amount of bromodeoxyuridine (BrdUrd) into DNA, followed by mutagenic treatment and subsequent culture for second and third generations of BrdUrd incorporation for the scoring of sister chromatid exchanges (SCEs) per cell cycle in three-way differentially (TWD) stained chromosomes, has been used to investigate the possible cancellation of SCEs. Cancellation is expected to occur if two mutagen-induced SCEs occur at exactly the same site in subsequent rounds of replication. Lesions in DNA seem to persist and are able to induce SCE throughout two cell cycles after treatment with the three mutagens tested--mitomycin C (MMC), ethyl methanesulfonate (EMS) and ultraviolet (UV) light--though this latter agent was shown as only moderately persistent. Our results seem to indicate that SCEs induced by these mutagens do not take place at the same locus in successive cell generations, as assessed by a lack of SCE cancellation.
Environ Mol Mutagen 1994
PMID:Evidence that SCEs induced by mutagens do not occur at the same locus in successive cell cycles: lack of cancellation in three-way stained CHO chromosomes. 752 77

Spontaneous and induced mutations at the HPRT locus were analyzed in one normal (MRC5CV1) and one ataxia telangiectasia (AT5BIVA) SV40-transformed cell line derived from male donors. Multiplex PCR and Southern analyses revealed a high frequency of spontaneous deletion mutations that may be a consequence of the SV40 transformation. Four mutagens (ethyl methanesulfonate, bromodeoxyuridine, bleomycin, adriamycin), which differ in their types of primary DNA lesions, caused specific patterns of mutations. By using fluorescence in situ hybridization (FISH) techniques, we were able to show that more than 90% of the AT5BIVA cells contained two X chromosomes with HPRT alleles, while in more than 90% of the MRC5CV1 cells genomic hemizygosity for the HPRT gene was found. Taking into account these findings we found that the AT5BIVA cell line possesses spontaneous hypermutability as well as hypersensitivity and hypermutability to bleomycin (BLM) and adriamycin (AM). Both mutagens induced deletion mutations in both cell lines, but more complex mutations and larger deletions were found in AT5BIVA cells.
Somat Cell Mol Genet 1994 Nov
PMID:Characterization of spontaneous and induced mutations in SV40-transformed normal and ataxia telangiectasia cell lines. 753 43

Phytochrome is the red/far-red absorbing photoreceptor active in photomorphogenesis, the apoprotein of which is encoded by a small gene family (PHYA, PHYB, PHYC, PHYD and PHYE). A novel phytochrome B-deficient mutant, phyB-103, was isolated from a screen of EMS-mutagenised Arabidopsis M2 seed. phyB-103 carries a G-to-A base substitution at the 5' splice site +1 G nucleotide of intron 1 of PHYB. The phyB-103 PHYB transcript is larger than the wild-type PHYB transcript and DNA sequence analysis showed that the entire intron is retained in the mature PHYB transcript of phyB-103. Thus the phyB-103 G-to-A substitution prevents intron splicing. The retained intron contains within it an in-frame stop codon, and the predicted PHYB-003 apoprotein thus terminates prematurely. phyB-103 is therefore likely to be a null allele of PHYB, consistent with the observation that the phenotype conferred by phyB-103 is as severe as that conferred by previously described phyB null alleles.
Plant Mol Biol 1995 Mar
PMID:Impaired splicing of phytochrome B pre-mRNA in a novel phyB mutant of Arabidopsis. 753 7

The PHO85 gene of Saccharomyces cerevisiae encodes a cyclin-dependent kinase involved in both transcriptional regulation and cell cycle progression. Although a great deal is known concerning the structure, function, and regulation of the highly homologous Cdc28 protein kinase, little is known concerning these relationships in regard to Pho85. In this study, we constructed a series of Pho85-Cdc28 chimeras to map the region(s) of the Pho85 molecule that is critical for function of Pho85 in repression of acid phosphatase (PHO5) expression. Using a combination of site-directed and ethyl methanesulfonate-induced mutagenesis, we have identified numerous residues critical for either activation of the Pho85 kinase, interaction of Pho85 with the cyclin-like molecule Pho80, or substrate recognition. Finally, analysis of mutations analogous to those previously identified in either Cdc28 or cdc2 of Schizosaccharomyces pombe suggested that the inhibition of Pho85-Pho80 activity in mechanistically different from that seen in the other cyclin-dependent kinases.
Mol Cell Biol 1995 Oct
PMID:Structure-function relationships of the yeast cyclin-dependent kinase Pho85. 756 99


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