Showing papers on "Mutant published in 1980"
TL;DR: Electron microscopy of sec mutant cells reveals the temperature-dependent accumulation of membrane-enclosed secretory organelles, and it is suggested that these structures represent intermediates in a pathway in which secretion and plasma membrane assembly are colinear.
1,703 citations
TL;DR: Mutants of Chinese hamster ovary cells lacking dihydrofolate reductase were isolated after mutagenesis and exposure to high-specific-activity [3H]deoxyuridine as a selective agent.
Abstract: Mutants of Chinese hamster ovary cells lacking dihydrofolate reductase (tetrahydrofolate dehydrogenase, 7,8-dihydrofolate:NADP+ oxidoreductase; EC 1.5.1.3) activity were isolated after mutagenesis and exposure to high-specific-activity [3H]deoxyuridine as a selective agent. Fully deficient mutants could not be isolated starting with wild-type cells, but could readily be selected from a putative heterozygote that contains half of the wild-type level of dihydrofolate reductase activity. The heterozygote itself was selected from wild-type cells by using [3H]deoxyuridine together with methotrexate to reduce intracellular dihydrofolate reductase activity. Fully deficient mutants require glycine, a purine, and thymidine for growth; this phenotype is recessive to wild type in cell hybrids. Revertants have been isolated, one of which produces a heat-labile dihydrofolate reductase activity. These mutants may be useful for metabolic studies relating to cancer chemotherapy and for fine-structure genetic mapping of mutations by using available molecular probes for this gene.
1,421 citations
TL;DR: In this paper, a reduced sensitivity to the inhibitory action of white light on hypocotyl elongation was observed in 41 mutants induced in Arabidopsis tbaliana at 5 different loci.
736 citations
TL;DR: The system of non-germinating mutants offers a resolving power unique in higher plants, so that self-detecting rare events like induced revertants or intragenic recombinants can be efficiently screened for.
Abstract: In Arabidopsis thaliana 37 independent irradiation or EMS induced mutants were isolated which have an absolute or almost absolute gibberellin (GA) requirement for germination and successive elongation growth. These are called 'non-germinating GA-dwarfs', since without further addition of GA they develop into typical GA-dwarfs, being dark green, stunted and sterile. However, with repeated GA-treatment they develop into fertile plants with a completely wild type phenotype, or nearly so. In addition, 19 independently induced 'germinating GA-dwarfs' were obtained, i.e. mutants which do germinate without GA but develop into typical GA-dwarfs. With repeated GA-treatment these too grow to become completely wild type phenotypes, or nearly so. 'Germinating dwarfs' have been found by previous authors in a number of other plant species. The 'non-germinating dwarfs' form a new class of mutants. The system of non-germinating mutants offers a resolving power unique in higher plants, so that self-detecting rare events like induced revertants or intragenic recombinants can be efficiently screened for.The 56 GA-sensitive mutants represent mutations at 5 loci, located on three of five Arabidopsis chromosomes. At three of the five loci both mutant classes were represented in similar frequency ratio's, whilst at the other two loci only germinating dwarfs were found.
687 citations
TL;DR: Mutants of Agrobacterium tumefaciens which affect virulence or the ability to catabolize octopine were isolated after Tn5-induced mutagenesis, and three mutants contained insertions in the T-deoxyribonucleic acid.
Abstract: Mutants of Agrobacterium tumefaciens which affect virulence or the ability to catabolize octopine were isolated after Tn5-induced mutagenesis. Of 8,900 colonies tested, 7 mutants with Tn5 insertions in a specific region of other Ti plasmid unable to catabolize octopine were isolated. Thirty-seven mutants affected in tumorigenesis resulted from insertions in the Ti plasmid and the Agrobacterium chromosome. Of these mutations, 12 were chromosomal and 25 mapped on the plasmid. Twenty-three mapped within a 20-megadalton region, which is distinct from the Ti plasmid sequences found stably integrated into the plant cell genome T-deoxyribonucleic acid). Included in these were mutants that were either a virulent or produced tumors with unusual morphologies. Three mutants contained insertions in the T-deoxyribonucleic acid. These three mutants incited tumors which synthesized octopine but had an altered morphology due to either extensive proliferation of shoots or roots from the tumor callus. Three additional mutants not caused by Tn5 contained mutations in the Ti plasmid.
429 citations
TL;DR: It is postulated that VP175 is involved in the transition from immediate early to earlyprotein synthesis, requird continuously to maintain early protein synthesis, and autoregulated, acting to inhibit immediate early proteinhesis.
Abstract: Herpes simplex virus (HSV)-specific proteins fall into at least three kinetic classes whose synthesis is sequentially and coordinaely regulated Temperature-sensitive (ts) mutants of one complementation group (1-2) are defective in the transition from immediate early to early and late protein synthesis To elucidate the function of the 1-2 gene product in the HSV type 1 replicative cycle, nine ts mutants in this group were mapped by fine-structure analysis and characterized members of the group lie within the terminally repeated sequences of the S region of the genome Fine-structure genetic and physical mapping permitted the mutations to be ordered within these sequences Because it has been shown that the message for VP175 and the DNA template specifying this protein extend beyond the limits of the physical map of the mutations, it follows that the mutations must lie within the structural gene for VP175 Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis showed that most members of the group overproduced the immediate early proteins VP175, -136, -110, and -63 and markedly underproduced early and late proteins at the nonpermissive temperature In temperature shiftup experiments, it was fund that the synthesis of early and late proteins ceased, whereas the synthesis of immediate early proteins began again Thus, it is postulated that VP175 is (i) involved in the transition from immediate early to early protein synthesis, (ii) requird continuously to maintain early protein synthesis, (iii) autoregulated, acting to inhibit immediate early protein synthesis
411 citations
TL;DR: Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized, suggesting that their phenotypes result from the complete absence of gene activity.
Abstract: Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.
404 citations
TL;DR: By demonstrating the presence of hamster gene sequences in transformants, the use of this gene may allow the introduction and amplification of virtually any genetic element in various new cellular environments.
Abstract: We have transferred a mutant hamster gene coding for an altered dihydrofolate reductase to wild-type cultured mouse cells by using total genomic DNA from methotrexate-resistant Chinese hamster ovary A29 cells as donor By demonstrating the presence of hamster gene sequences in transformants we have provided direct evidence for gene transfer Transformants selected for increased resistance to methotrexate contain increased amounts of the newly transferred gene We have used this mutant dhfr gene to introduce the Escherichia coli antibiotic resistance plasmid pBR322 into animal cells Amplification of the dhfr sequences results in amplification of the pBR322 sequences as well The use of this gene may allow the introduction and amplification of virtually any genetic element in various new cellular environments
393 citations
TL;DR: The possible roles of wee1 and cdc2 in the mitotic control are discussed, with particular reference to the part they may play in the monitoring of cell growth rate and the timing of mitosis, both of which influence the timingof mitosis.
Abstract: Fifty-two wee mutants that undergo mitosis and cell division at a reduced size compared with wild type have been genetically analyzed. The mutants define two genes, wee1 and cdc2 , which control the timing of mitosis. Fifty-one of the mutants map at the wee1 locus, which is unlinked to any known cdc gene. One of the wee1 alleles has been shown to be nonsense suppressible. The 52nd wee mutant maps within cdc2 . Previously, only temperature-sensitive mutants that become blocked at mitosis have been found at the cdc2 locus. The simplest interpretation of these observations is that wee1 + codes for a negative element or inhibitor, and cdc2 + codes for a positive element or activator in the mitotic control. The gene dosage of wee1 + plays some role in determining the timing of mitosis, but the gene dosage of cdc2 + has little effect. However, some aspect of the cdc2 gene product activity is important for determining when mitosis takes place. The possible roles of wee1 and cdc2 in the mitotic control are discussed, with particular reference to the part they may play in the monitoring of cell size and cell growth rate, both of which influence the timing of mitosis.
381 citations
TL;DR: Triton gel electrophoresis provides rapid analysis of very small amounts of haemoglobin, and permits examination of globin chain composition as well as globin synthetic ratios.
Abstract: Separation of globin chains by electrophoresis provides a simple and rapid method for the determination of the G gamma/A gamma ratio in human fetal haemoglobin, and of biosynthetic rates of the globin chains. Whole haemolysates were analysed by electrophoresis on polyacrylamide gels in urea, acetic acid and Triton X-100. Electrophoresis of haemolysates from newborn infants led to four bands: A gamma, G gamma, beta and alpha. The identity of these bands was indicated by examination of haemoglobins of known globin chain composition. In 15 samples, the % G gamma was similar by Triton gels and by amino acid analysis of the gamma CB-3 peptide. Some mutant globin chains were also separable with the electrophoretic technique. Triton gel electrophoresis provides rapid analysis of very small amounts of haemoglobin, and permits examination of globin chain composition as well as globin synthetic ratios.
375 citations
TL;DR: Thirty-three temperature-sensitive mutations defective in the start event of the cell division cycle of Saccharomyces cerevisiae were isolated and subjected to preliminary characterization, revealing single nuclear genes, unlinked to one another.
Abstract: Thirty-three temperature-sensitive mutations defective in the start event of the cell division cycle of Saccharomyces cerevisiae were isolated and subjected to preliminary characterization. Complementation studies assigned thes mutations to four complementation groups, one of which, cdc28, has been described previously. Genetic analysis revealed that these complementation groups define single nuclear genes, unlinked to one another. One of the three newly identified genes, cdc37, has been located in the yeast linkage map on chromosome IV, two meiotic map units distal to hom2.--Each mutation produces stage-specific arrest of cell division at start, the same point where mating pheromone interrupts division. After synchronization at start by incubation at the restrictive temperature, the mutants retain the capacity to enlarge and to conjugate.
TL;DR: It is argued that the T-A-T-A -A-A and A-G-A motif is a specificity element, a selector of eukaryotic gene transcription, and that deletion of H2A gene-specific conserved DNA sequences upstream from this motif enhanced mRNA synthesis.
Abstract: Conserved DNA sequence elements of putative regulatory functions were deleted from the prelude region of a sea urchin H2A histone gene. For this, the wild-type H2A gene of the 6-kilobase histone DNA repeat unit was replaced by various mutant H2A genes by cloning. The effects of the manipulation on H2A mRNA synthesis were studied by injection of the mutant DNAs into centrifuged Xenopus oocytes. The unmanipulated H2B gene residing within the same repeat unit provided a suitable internal control for these studies. Deletion of the T-A-T-A-A-A-T-A motif, once thought to be the functional equivalent of the bacterial Pribnow box, did not abolish transcription of the gene; instead, a number of novel mRNA 5' termini were generated. We argue that the T-A-T-A-A-A-T-A motif is a specificity element, a selector of eukaryotic gene transcription. Deletion of the "cap-sequence," 5' pyrimidine-C-A-T-T-C-purine 3' and most of the mRNA leader sequence did not abolish transcription but created yet another mRNA 5' terminus. In contrast to these deletions, which are both down-mutations, deletion of H2A gene-specific conserved DNA sequences upstream from the T-A-T-A-A-A-T-A motif enhanced mRNA synthesis. A hypothesis for the function of these DNA sequences as eukaryotic promoter elements is discussed.
TL;DR: Analysis of the DNA sequence has revealed that in the strain D273-10B, the cytochrome b gene is composed of three exons, which is somewhat less complex than has been reported for other yeast strains i which exon b1 appears to be further fragmented into three smaller exons.
TL;DR: Pseudomonas aeruginosa PAO mutants defective in elastase were isolated by plate assays of nitrosoguanidine-mutagenized clones and one mutant (PAO-E64) was apparently identical to the parental strain except for its deficiency inElastase activity.
Abstract: Pseudomonas aeruginosa PAO mutants defective in elastase were isolated by plate assays of nitrosoguanidine-mutagenized clones. A total of 75 elastase mutants were isolated from 43,000 mutagenized clones. One mutant (PAO-E64) was apparently identical to the parental strain except for its deficiency in elastase activity. This mutant produced an enzyme which was antigenically indistinguishable from parental elastase. Furthermore, equal levels of elastase antigen were produced by this mutant and its parental strain. The mutant elastase, however, had greatly reduced enzymatic activity. Mutant PAO-E64 is presumed to have a mutation in the structural gene for elastase. We have designated the genotype of the mutation in PAO-E64 as lasA1.
TL;DR: Temperature-sensitive mutations that produce insensitivity to division arrest by alpha-factor, a mating pheromone, were isolated in an MATa strain of Saccharomyces cerevisiae and shown by complementation studies to difine eight genes.
Abstract: Temperature-sensitive mutations that produce insensitivity to division arrest by alpha-factor, a mating pheromone, were isolated in an MATa strain of Saccharomyces cerevisiae and shown by complementation studies to difine eight genes. All of these mutations (designated ste) produce sterility at the restrictive temperature in MATa cells, and mutations in seven of the genes produce sterility in MAT alpha cells. In no case was the sterility associated with these mutations coorectible by including wild-type cells of the same mating type in the mating test nor did nay of the mutants inhibit mating of the wild-type cells; the defect appears to be intrinsic to the cell for mutations in each of the genes. Apparently, none of the mutants is defective exclusively in division arrest by alpha-factor, as the sterility of none is suppressed by a temperature-sensitive cdc 28 mutation (the latter imposes division arrest at the correct cell cycle stage for mating). The mutants were examined for features that are inducible in MATa cells by alpha-factor (agglutinin synthesis as well as division arrest) and for the characteristics that constitutively distinguish MATa from MAT alpha cells (a-factor production, alpha-factor destruction). ste2 Mutants are defective specifically in the two inducible properties, whereas ste4, 5, 7, 8, 9, 11, and 12 mutants are defective, to varying degrees, in constitutive as well as inducible aspects. Mutations in ste8 and 9 assume a polar budding pattern unlike either MATa or MAT alpha cells but characteristic of MATa/alpha cells. This study defines seven genes that function in two cell types (MATa and alpha) to control the differentiation of cell type and one gene, ste2, that functions exclusively in MATa cells to mediate responsiveness to polypeptide hormone.
TL;DR: Results show that the carboxy-terminal amino acid sequence of beta-lactamase is essential to successful transport across the cytoplasmic membrane, and suggest that the presence (and probably also the act of removal) of the signal sequence does not suffice to ensure secretion.
TL;DR: The his4-912 mutation results from insertion of a 6200 bp transposable element into the his4 gene of yeast and carries a number of chromosomal aberrations including deletions, translocations, a transposition and an inversion.
TL;DR: Although these mutants resemble xeroderma pigmentosum human mutants with respect to their repair defect and cross-sensitivity to the carcinogen 4-nitroquinoline-1-oxide, one of two clones is characterized by extreme hypersensitivity to MMC (80-fold as compared to the wild type).
Abstract: A simple procedure for isolating mutagen-sensitive clones of CHO cells was developed and applied in mutant hunts in which colonies were screened for hypersensitivity to killing by ultraviolet radiation (UV, ethyl methanesulfonate (EMS), or mitomycin C (MMC). Each of two UV-sensitive clones studied in detail had a D37 dose of 1.0 J/m2 compared to 7.0 J/m2 for the wild-type cells, and each was shown to have no detectable repair replication following exposure to UV doses of up to 26 J/m2. Although these mutants resemble xeroderma pigmentosum human mutants with respect to their repair defect and cross-sensitivity to the carcinogen 4-nitroquinoline-1-oxide, one of two clones (UV-20) is characterized by extreme hypersensitivity to MMC (80-fold as compared to the wild type). Clones having hypersensitivity to alkylating agents, but not UV, were obtained using MMC and EMS. In the latter case the two clones had significantly increased sensitivity to the killing action of 60Co gamma-rays.
TL;DR: Two distinct loci that confer resistance to acycloguanosine (acyclo-Guo) in herpes simplex virus types 1 have been identified and suggest that resistance to both drugs is specified by a mutant DNA polymerase.
Abstract: Two distinct loci that confer resistance to acycloguanosine (acyclo-Guo) in herpes simplex virus types 1 have been identified. The first locus is the gene for the virus-specific thymidine kinase (TK). Mutations that decrease TK activity also render the virus resistant to acyclo-Guo, and the level of resistance corresponds to the decrease in TK activity. acyclo-Guo resistance due to defective TK expression is recessive to the wild-type phenotype, acyclo-Guo-sensitive (ACGs). We term this locus ACGr-TK. The second locus is defined by the properties of a mutant, PAAr5, which is resistant to acyclo-Guo and to phosphonoacetic acid (PAA) yet exhibits wild-type TK activity. The acyclo-Guo-resistant locus in PAAr5 is separable from ACGr-TK mutations by recombination. Moreover, PAAr5 and ACGr-TK mutants can complement each other, producing drug-sensitive gene products which result in growth inhibition in the presence of acyclo-Guo. The acyclo-Guo resistance conferred by PAAr5 behaves as though it were codominant with the wild-type phenotype. This second acyclo-Guo-resistance locus is closely linked to the mutation specifying resistance to PAA. Resistance to PAA is thought to result from mutations in the gene for viral DNA polymerase. Thus, the close linkage of the ACGr and PAAr loci suggest that resistance to both drugs is specified by a mutant DNA polymerase. We term this second locus ACGr-PAA.
TL;DR: It was found that, in normal females, the genes for c36, c38, and at least one other chorion protein are specifically amplified more than 10-fold in the DNA of late-stage egg chambers, suggesting that altered gene dosage may be responsible for the decreased synthesis of chorions in the mutant.
Abstract: The endochorion and exochorion of Drosophila eggs are synthesized by the ovarian follicle cells during a brief period of about 5 hr. In this terminal phase of egg chamber development, the structural genes for several abundant chorion proteins are expressed at high levels according to a temporally regulated program. The female-sterile mutation ocelliless maps at the site of the genes for two of these proteins, the 36,000- and 38,000-dalton chorion proteins (c36 and c38), which are closely linked. The mutation results in a cis-acting reduction in the amounts of c36 and c38 that accumulate in late-stage egg chambers. We have investigated the mechanism that underlies this decreased production by using cDNA clones complementary to these gene sequences. Unexpectedly, it was found that, in normal females, the genes for c36, c38, and at least one other chorion protein are specifically amplified more than 10-fold in the DNA of late-stage egg chambers. The extra replication involves at least some adjacent chromosomal sequences and begins prior to the onset of mRNA and protein synthesis. The additional DNA remains stable after gene expression has ceased. The behavior of these genes is thus reminiscent of the properties of the DNA puffs that have been described in several groups of Diptera. The extent of amplification of c36 and c38, but not of the 18,000-dalton chorion protein c18 (which is unlinked), was decreased in the egg chambers of flies homozygous for ocelliless, suggesting that altered gene dosage may be responsible for the decreased synthesis of chorion proteins in the mutant.
TL;DR: In the small nematode, Caenorhabditis elegans, mutants with a disorganized myofilament lattice structure have been identified by polarized light and electron microscopy and phenotypes are described for the mutants from the 9 complementation groups not previously reported on.
TL;DR: Tn5's ability to turn on distal gene expression is not due to a promoter in its central region and therefore is not dependent on the overall orientation of Tn5 in the operon.
Abstract: We assessed the effect of insertions of the kanamycin resistance transposon Tn5 in the lac operon of Escherichia coli on the expression of distal genes lacY and lacA (melibiose fermentation at 41 degrees C and thiogalactoside transacetylase synthesis, respectively). Every insertion mutation tested (41 in lacZ and 23 in lacY) was strongly polar. However, approximately one-third of the insertion mutants expressed distal genes at low levels due to a promoter associated with Tn5. To localize this promoter, we (i) reversed the orientation of Tn5 at several sites and (ii) replaced wild-type Tn5 with several substitution derivatives which lack Tn5's central region. Neither alteration changed the expression of distal genes. Thus, in contrast to transposons IS2 and TnA. Tn5's ability to turn on distal gene expression is not due to a promoter in its central region and therefore is not dependent on the overall orientation of Tn5 in the operon. Our results suggest that the promoter is within 186 base pairs of the ends of Tn5. It is possible that the promoter is detected in only a fraction of insertions because it overlaps Tn5-target sequence boundary.
TL;DR: In this article, it was shown that Pseudomonas aeruginosa cells grown in Mg2+-deficient medium acquire nonmutational resistance to the chelator ethylenediaminetetraacetate and to the cationic antibiotic polymyxin B; this type of resistance can be reversed by transferring the cells to Mg 2+-sufficient medium for a few generations.
Abstract: It is well established that Pseudomonas aeruginosa cells grown in Mg2+-deficient medium acquire nonmutational resistance to the chelator ethylenediaminetetraacetate and to the cationic antibiotic polymyxin B; this type of resistance can be reversed by transferring the cells to Mg2+-sufficient medium for a few generations. Stable mutants resistant to polymyxin B were isolated and shown to have also gained ethylenediaminetetraacetate resistance. Both the mutants and strains grown on Mg2+-deficient medium had greatly enhanced levels of outer membrane protein H1 when compared with the wild-type strain or with revertants grown in Mg2+-sufficient medium. It was determined that in all strains and at all medium Mg2+ concentrations, the cell envelope Mg2+ concentration varied inversely with the amount of protein H1. In addition, the increase in protein H1 in the mutants was associated with an increase in resistance to another group of cationic antibiotics, the aminoglycosides, e.g., gentamicin. We propose that protein H1 acts by replacing Mg2+ at a site on the lipopolysaccharide which can otherwise be attacked by the cationic antibiotics or ethylenediaminetetraacetate.
TL;DR: The importance of the viral DNA polymerase region in mediating acyclo-Guo resistance is suggested and is consistent with a close relationship between the PAAr mutation site and the AGGr locus.
Abstract: Acycloguanosine [9-(2-hydroxyethoxymethyl)guanine; acyclo-Guo] is a potent inhibitor of herpes simplex viruses (HSV); it is selectively phosphorylated in virus-infected cells. In order to define those viral functions that may mediate resistance to acyclo-Guo, the drug sensitivities of temperature-sensitive (ts) and phosphonoacetic acetic acid (PAA)-resistant mutants of HSV-1 and HSV-2 have been determined. Two distinct viral genetic loci are independently associated with acyclo-Guo resistance. Mutations resulting in diminished thymidine kinase activity are associated with resistance to inhibition by acyclo-Guo. Several PAA-resistant viruses that express wild-type levels of thymidine kinase activity are also resistant to acyclo-Guo. This suggests the importance of the viral DNA polymerase region in mediating acyclo-Guo resistance and is consistent with a close relationship between the PAAr mutation site and the AGGr locus. When wild-type HSV-1 is serially propagated under the selective pressure of acyclo-Guo, rapid emergence of resistant virus occurs, accompanied by the simultaneous appearance of thymidine kinase-deficient progeny.
TL;DR: Thy-1mutant mouse lymphoma cells have the a1,3-mannosyltransferase necessary for the conversion of the Man5GlCNAcz species to Man,GlcNAcz, but lack the appropriate mannosy1 donor (dolichol-P-mannose)necessary for the formation of the larger lipid-linked oligosaccharides.
TL;DR: The amino acid composition and sequence deduced from the DNA sequence indicate that the protein is very hydrophobic, with three long domains (greater than 30 residues) consisting of nonpolar amino acids.
TL;DR: Some of the genes controlling start by isolating mutants which are altered with respect to the conditions in which start occurs are identified, including whi-2, which is involved in the mechanism whereby cells arrest in G1 in stationary phase.
Abstract: In many eukaryotes it is thought that cell proliferation is regulated at a point in G1 close to the initiation of DNA synthesis1. Hartwell2,3 and his colleagues have shown such a point in G1 phase in the budding yeast, Saccharomyces cerevisiae, defined by the cdc 28 mutation. He has termed this point ‘start’ and showed that for cells to proceed beyond start, initiate DNA synthesis and produce a bud, various conditions must be met. Two of these conditions are the presence of adequate nutrients in the medium and the attainment of a critical size. We identify here some of the genes controlling start by isolating mutants which are altered with respect to the conditions in which start occurs. Two types of mutant have been isolated. One results in bud initiation when the parent cell is only half the size at which bud initiation occurs in wild-type cells. Such mutants define a single gene, whi-1, and they are apparently analogous to the size mutants isolated by Nurse and his colleagues4–6 in Schizosaccharomyces pombe. A second type of mutation affects a second gene, whi-2, which is involved in the mechanism whereby cells arrest in G1 in stationary phase. whi-2− cells growing exponentially initiate buds at the same size as wild-type cells. In stationary phase, however, whi-2− cells, unlike wild-type cells, are predominantly budded and are smaller than wild-type cells.
TL;DR: By functional tests of in vitro mutated histone DNA in the Xenopus oocyte, it is discovered that the segment E of the A+T-rich spacer DNA lying at a considerable distance upstream of the conservative T-A-T-A of the H2A gene transcription is a strong modulator element of H2a gene transcription.
Abstract: The control region of a sea urchin H2A histone gene may be functionally dissected into at least three DNA segments, which we have termed modulator, selector, and initiator elements. While the initiator and in particular the selector containing the T-A-T-A-A-A-T-A sequence are specificity elements that dictate the generation of faithful 5' ends to H2A mRNA, the modulators control the rate at which these specificity elements operate [Grosschedl, R. & Birnstiel, M. L. (1980) Proc. Natl. Acad. Sci. USA 77, 1432-1436]. By functional tests of in vitro mutated histone DNA in the Xenopus oocyte we have now discovered that the segment E of the A+T-rich spacer DNA lying at a considerable distance upstream of the conservative T-A-T-A-A-A-T-A sequence is a strong modulator element of H2A gene transcription. Deletion of this element creates a 15- to 20-fold H2A-specific down mutation. Segment E by itself cannot elicit initiation of transcription except in coordination with the prelude sequence of the H2A gene. The nucleotide sequence of the relevant spacer element showing modulator activity has been determined and found to contain a pattern of T and A runs as well as a series of inverted repeats. Additional pre-H2A spacer mutants, including a spacer inversion mutant, have been constructed in vitro, that, when injected into the oocyte nucleus, modulate the expression of the H2A gene by an overall factor as large as 100. Other factors controlling promoter activity are discussed.
TL;DR: The cho1 mutant appears to use almost exclusively the alternative pathway described by Kennedy and Weiss (1956) J. Biol.
TL;DR: It is expected that the latter types, the Miros group, will soon completely supersede the spontaneous or radiation-induced Horim sports and mutants and take over the leading position of the Horim group in the production of all-year-round (AYR) cut flowers.
Abstract: Radiation-induced sports in Chrysanthemum morifolium Ram. have been reported for several years. It has become an everyday practice to produce flower-colour mutants from outstanding cross-breeding products, even before they are distributed for the commercial production of cut flowers.