Single Gene Differences Research Articles

Comprehensive analysis to identify pseudogenes/lncRNAs-hsa-miR-200b-3p-COL5A2 network as a prognostic biomarker in gastric cancer

ObjectiveGastric cancer is one of the most common and deadly types of cancer. The molecular mechanism of gastric cancer progression remains unclear.Materials and methodsFour hub genes were identified through GEO and TCGA database screening and analysis. Prognostic analysis revealed that COL5A2 was the most likely to affect the prognosis of gastric cancer among the four hub genes. The relationships between COL5A2 and clinical variables and immune cell infiltration were analyzed. Then, COL5A2 was analyzed for single-gene differences and related functional enrichment. Using the starBase database for prediction and analysis, miRNAs and pseudogenes/lncRNAs that might combine with COL5A2 were identified; thus, the ceRNA network was constructed. Finally, the network was verified by Cox analysis and qPCR, and a nomogram was constructed.ResultsFirst, we found that COL5A2, COL12A1, BGN and THBS2 were highly expressed in gastric cancer. COL5A2 had statistical significance in overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) analysis. Immune infiltration analysis suggested that COL5A2 might influence the changes in the tumor immune microenvironment. The StarBase database was used to predict that 3 pseudogenes and 7 lncRNAs might inhibit the hsa-miR-200b-3p-COL5A2 axis in gastric cancer. The pseudogenes/lncRNA-hsa-miR-200b-3p-COL5A2 ceRNA network was identified and verified using Cox regression analysis and PCR. Finally, we constructed a nomogram.ConclusionsWe elucidated the regulatory role of the pseudogenes/lncRNA-hsa-miR-200b-3p-COL5A2 network in gastric cancer progression and constructed a nomogram. These studies may provide effective treatments and potential prognostic biomarkers for gastric cancer.

A primary study on genes with selected mutations by in vitro passage of Chlamydia muridarum strains.

This study is to investigate the functions of newly discovered genes in Chlamydia muridarum (C. muridarum) strains with single gene differences. Using whole genome sequencing and plaque formation assays, C. muridarum parental and passaging strains were established, and the isogenic clones expressing certain genotypes were isolated. Strains with single gene differences were obtained. Based on prediction, the valuable strains with single gene differences of tc0412, tc0668 or tc0237 were subjected to the in vitro and in vivo experiments for biological characterization and virulence analysis. Insertional -472840T mutation of the tc0412 gene (T28T/B3 type) matching with the nonmutant tc0668 gene and tc0237 gene with point mutations G797659T (Q117E) might slow the growth of Chlamydia due to the lack of a plasmid. The nonmutant tc0668 in the strain might induce a high incidence of hydrosalpinx in mice, while tc0668 with a G797659T point mutation was significantly attenuated. Compared with the nonmutant tc0237, the strains containing mutant tc0237 were characterized by reduced centrifugation dependence during infection. The identification and characterization of these genes might contribute to the comprehensive understanding of the pathogenic mechanism of Chlamydia.

Abstract P3-08-07: Distinct biological signatures describe differences in BRCA mutated subgroups

Abstract Background: BRCA mutated (BRCA+) breast cancers are expected to have increased activation of Homologous Recombination Deficiency (HRD) and altered DNA damage repair pathways when compared to BRCA wildtype (BRCA-). To better understand differences in these populations, biological patterns and immune responses to BRCA+ breast cancers were evaluated. The primary aim of our study was to use novel gene expression tools to assess early stage breast cancers with and without germline BRCA mutations, and within distinct BRCA+ subgroups. Methods: We identified 124 early stage untreated breast cancers with and without BRCA mutations (n = 62 and 62, respectively). Our BRCA- group was matched by hormone receptor (HR) status, age, and stage to the BRCA+ group. The NanoString Breast Cancer 360 panel was applied to RNA isolated from 80 breast tumors (BRCA+ = 39; BRCA- = 41). The BRCA+ group had a BRCA1+ subgroup (n=17) and a BRCA2+ subgroup (n=22). Results: There was a significant increase in two BC360 signatures in both the BRCA1+ and BRCA2+ tumors compared with the BRCA- population: Prosigna™Risk of Recurrence (ROR) score [BRCA1+: HR: 1.142 (95% CI 1.019, 1.279), p=0.02; BRCA2+: HR: 1.321 (95% CI 1.190, 1.466), p<0.001] and HRD [BRCA1+: HR: 3.576 (95% CI 2.174, 5.880), p=0.02; BRCA2+: HR: 1.801 (95% CI 1.142, 2.840), p<0.001]. BRCA1+ tumors had lower expression of ESR1 [p=0.03], PGR [p=0.02], ER signaling [p<0.001], and differentiation [p=0.005]; while BRCA2+ tumors had lower expression of stroma markers [p=0.02] and inflammatory chemokines [p=0.001]. The two BRCA+ subgroups had distinct molecular subtype correlation trends that were highly significant. BRCA1+ tumors were positively associated with a basal subtype [p<0.001], whereas this association was not significant for BRCA2+ tumors. BRCA2+ tumors were associated with an increase in luminal B subtype [p=0.05]. All BRCA+ tumors had a decrease in luminal A subtype correlation [BRCA1+: p<0.001; BRCA2+: p=0.002]. In addition to the BC360 signatures, a differential analysis of all genes in the BC360 panel revealed more single gene differences in BRCA2+ than BRCA1+ tumors when compared to BRCA- tumors. Conclusions: In early stage BRCA+ breast cancer, tumors have higher ROR and increased HRD signature scores compared to BRCA- tumors. Furthermore, BRCA1+ and BRCA2+ tumors have both signature and single gene expression differences when compared to BRCA- tumors, indicating distinct subgroup-related biology. The greater correlation of BRCA1+ tumors with basal-like biology and BRCA2+ tumors with aggressive hormonal biology confirms these trends. Distinctions in hormone receptor signaling, DNA-damage pathways, and microenvironment/inflammatory features between BRCA1 and BRCA2 associated cancers suggest a need for different prevention and therapeutic strategies for each of these breast cancer subtypes. The unique biological patterns identified here should be further evaluated as predictive or prognostic tools that could be translated into clinical care for early stage BRCA+ patients. Citation Format: Force J, Plichta J, Stashko I, Kimmick G, Westbrook K, Sammons S, Hwang S, Hyslop T, Kauff N, Castellar E, Nair S, Weinhold K, Davis S, Mashadi-Hossein A, Brauer HA, Marcom PK. Distinct biological signatures describe differences in BRCA mutated subgroups [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P3-08-07.

Memory of the vernalized state in plants including the model grass Brachypodium distachyon.

Plant species that have a vernalization requirement exhibit variation in the ability to “remember” winter – i.e., variation in the stability of the vernalized state. Studies in Arabidopsis have demonstrated that molecular memory involves changes in the chromatin state and expression of the flowering repressor FLOWERING LOCUS C, and have revealed that single-gene differences can have large effects on the stability of the vernalized state. In the perennial Arabidopsis relative Arabis alpina, the lack of memory of winter is critical for its perennial life history. Our studies of flowering behavior in the model grass Brachypodium distachyon reveal extensive variation in the vernalization requirement, and studies of a particular Brachypodium accession that has a qualitative requirement for both cold exposure and inductive day length to flower reveal that Brachypodium can exhibit a highly stable vernalized state.

Genetic endothelial systems biology of sickle stroke risk

AbstractGenetic differences in endothelial biology could underlie development of phenotypic heterogeneity among persons afflicted with vascular diseases. We obtained blood outgrowth endothelial cells from 20 subjects with sickle cell anemia (age, 4-19 years) shown to be either at-risk (n = 11) or not-at-risk (n = 9) for ischemic stroke because of, respectively, having or not having occlusive disease at the circle of Willis. Gene expression profiling identified no significant single gene differences between the 2 groups, as expected. However, analysis of Biological Systems Scores, using gene sets that were predetermined to survey each of 9 biologic systems, showed that only changes in inflammation signaling are characteristic of the at-risk subjects, as supported by multiple statistical approaches. Correspondingly, subsequent biologic testing showed significantly exaggerated RelA activation on the part of blood outgrowth endothelial cells from the at-risk subjects in response to stimulation with interleukin-1β/tumor necrosis factorα. We conclude that the pathobiology of circle of Willis disease in the child with sickle cell anemia predominantly involves inflammation biology, which could reflect differences in genetically determined endothelial biology that account for differing host responses to inflammation.

Genetic Influence on the Systems Biology of Sickle Stroke Risk Detected by Endothelial Gene Expression.

Stroke affects ∼10% of children with sickle cell anemia. There is evidence for a familial predisposition, and the strongest risk predictor is presence of Circle of Willis (CoW) disease. We hypothesize that inherited differences in endothelial biology influence whether or not the child with sickle cell anemia develops CoW disease. We have studied 20 subjects (age <20yr) with HbSS or HbSβ°thal. 11 are at-risk for stroke, defined as having had an actual stroke, or by having known CoW disease (TCD >200 cm/sec, or abnormal MRA); and 9 are not-at-risk, defined as having reached age 10 (at least) without a clinical stroke, plus having absence of CoW disease (TCD <150 cm/sec, or normal MRA). From each subject, a sample of blood outgrowth endothelial cells (BOEC) was prepared and used to obtain RNA for gene expression profiling (Affymetrix U133A platform). BOEC are a generic endothelial cell that reports constitutive endothelial phenotype. Preliminary studies established that there is a safe ‘window' of culture passage number after any acquired phenotypes have washed out and before BOEC become genetically unstable; all samples were evaluated at the same time point. The subjects revealed no significant single-gene differences between the 2 groups (by Welch t test, Wilcoxon test, or SAM). This was expected. Rather, we expect the genesis of CoW disease in different subjects to be influenced by various polymorphisms that impact similarly on the several biological systems relevant to cerebral vasculopathy (potentially, the biologies of redox, hypoxia, shear stress, adhesion, coagulation, inflammation, angiogenesis, vasoregulation, apoptosis). Using predetermined gene sets (having 79–156 members) for each biological system, we examined each gene's expression in terms of fold change relative to the average of the control samples, and used all genes on a given list to establish that system's ‘score' for each subject (generated such that down- and up-ward fold changes have equal impact and do not offset each other). Significant differences (Wald test) are noted between the at-risk and not-at-risk subjects for only 1 biological system: inflammation signaling (P=.0216). Multiple statistical approaches confirm this conclusion. Indirectly supporting the veracity of our findings, separation of the same 20 subjects into males vs females resulted in no group differences in biological systems scores. The strongest contributor transcripts to the inflammation score are proximate or distal to NFκB component RelA, and RelA response to inflammation (IL1+TNF) is seen to be greatly exaggerated for the at-risk BOEC samples. Genetically determined differences in endothelial biology probably help determine clinical phenotype of sickle cell anemia by influencing risk of developing CoW disease. Our data suggest that inflammation biology is the main biological system involved.

Recent Developments in the Detection of Fetal Single Gene Differences in Maternal Plasma and the Role of Size Fractionation

The presence of cell-free fetal DNA in maternal plasma allowed noninvasive prenatal diagnosis of fetal loci completely absent from the maternal genome, such as SRY gene and RhD gene. However, the detection of fetal point mutations is hindered by the predominance of maternal DNA sequences. Recent studies have shown that cell-free fetal DNA exists in maternal plasma in small fragments. Thus, cell-free fetal DNA can be enriched by size fractionation, which improves detection of fetal gene mutations. Furthermore, it has been shown that Matrix Assisted Laser Desorption Ionization Time-of-Flight (MALDI-TOF) mass spectrometry also permits the detection of fetal SNPs from maternal plasma. These two new developments are discussed.

Genetic influence on the systems biology of sickle stroke risk detected by endothelial gene expression

About 10% of children with sickle cell anemia are at risk for stroke due to presence of Circle of Willis (CoW) disease. We studied 20 adolescents with HbSS or HbSβ°thal: 12 have CoW disease and are at-risk for stroke, 8 are not-at-risk. From each subject, a sample of blood outgrowth endothelial cells (BOEC) was prepared and used to obtain RNA for gene expression profiling (Affymetrix U133A platform). Preliminary studies established that valid data can be obtained using this method. Our 20 subjects had no significant single-gene differences between the 2 groups (by multiple tests). This was expected because we expect the genesis of CoW disease in different subjects to be influenced by various polymorphisms that impact similarly on the 9 biological systems relevant to cerebral vasculopathy. Using predetermined gene lists (having 79–156 members) for each biological system, we examined each gene's expression in terms of fold change relative to the average of the control samples, and used all genes on a given list to establish that system's ‘score’ for each subject (generated such that down- and upward fold changes have equal impact and do not offset each other). Significant differences (Wald test) are noted between the at-risk and notat-risk subjects for 3 biological systems: adhesion (P<.002), hypoxia (P<.002), and inflammation (P=.0005). Use of vectorial analysis to simultaneously test multiple systems shows that adhesion + hypoxia + inflammation strongly discriminates between at-risk and not-at-risk subjects (P=.00001). Genetically determined differences in endothelial biology probably help determine clinical phenotype of sickle cell anemia by influencing risk of developing CoW disease.

Genetic Influence on the Systems Biology of Sickle Stroke Risk Detected by Endothelial Gene Expression.

Stroke affects ~10% of children with sickle cell anemia. There is evidence for a familial predisposition, and the strongest risk predictor is presence of Circle of Willis (CoW) disease. We hypothesize that inherited differences in endothelial biology influence whether or not the child with sickle cell anemia develops CoW disease. We have studied 20 subjects (ages 10–18) with HbSS or HbSβothal. Twelve are at-risk for stroke, defined as having had an actual stroke, or by having known CoW disease (TCD >200 cm/sec, or abnormal MRA); and 8 are not-at-risk, defined as having reached age 10 (at least) without a clinical stroke, plus having absence of CoW disease (TCD <150 cm/sec, or normal MRA). From each subject, a sample of blood outgrowth endothelial cells (BOEC) was prepared and used to obtain RNA for gene expression profiling (Affymetrix U133A platform). BOEC are a generic endothelial cell that reports constitutive endothelial phenotype. Preliminary studies established that there is a safe ‘window' of culture passage number after any acquired phenotypes have washed out and before BOEC become genetically unstable; all samples were evaluated at the same time point. Our 20 subjects revealed no significant single-gene differences between the 2 groups (by Welch t test, Wilcoxin test, or SAM). This was expected, as it is highly improbable that a 10% prevalence of CoW disease would be accounted for by co-inheritance of one other single gene disorder. Rather, we expect the genesis of CoW disease in different subjects to be influenced by various polymorphisms that impact similarly on the several biological systems relevant to cerebral vasculopathy (potentially, the biologies of redox, hypoxia, shear stress, adhesion, coagulation, inflammation, angiogenesis, vasoregulation, apoptosis). Using predetermined gene lists (having 79–156 members) for each biological system, we examined each gene's expression in terms of fold change relative to the average of the control samples, and used all genes on a given list to establish that system's ‘score' for each subject (generated such that down- and up-ward fold changes have equal impact and do not offset each other). Significant differences (Wald test) are noted between the at-risk and not-at-risk subjects for 3 biological systems: adhesion (P<.002), hypoxia (P<.002), and inflammation (P=.0005). Use of vectorial analysis to simultaneously test multiple systems shows that adhesion + hypoxia + inflammation strongly discriminates between at-risk and not-at-risk subjects (P=.00001), and that further addition of coagulation gives strongest discrimination (P=0). Permutation testing most strongly supports inflammation as a discriminator. Indirectly supporting the veracity of our findings, separation of the same 20 subjects into males vs females resulted in no group differences in biological systems scores. Genetically determined differences in endothelial biology probably help determine clinical phenotype of sickle cell anemia by influencing risk of developing CoW disease. Our data suggest that specific biological systems are involved: adhesion, hypoxia, inflammation, and coagulation.

Ecological, practical, and political inputs into selection of weed targets: What makes a good biological control target?

The topic of ecological, practical, and political considerations in the selection of weed targets for biological control has been widely discussed during the past two decades, mostly from the perspective of insect herbivores. For conceptual and practical purposes, plant pathogens have been treated in these discussions as if they are a subset of inoculative biocontrol agents, with little said about the inherent differences between pathogens and insects as biocontrol agents or the selection of weed targets for control by the inundative, bioherbicide strategy. Herein, I attempt to address the question of what makes a good biological control target for plant pathogens used as inoculative as well as inundative agents, basing my analysis on examples from the past three decades. Despite the small number of examples available for this analysis, the following generalizations can be made: (1) Weeds with robust capacity for vegetative regeneration are more difficult to control with pathogens than those that lack this trait. (2) A plants growth habit is not a reliable guide for target selection; weeds that have been successfully controlled include annual and biennial herbs, perennial shrubs, perennial vines, and trees, while numerous failures have been reported irrespective of the targets growth habit or reproductive mode. (3) It is more challenging to control species with genetic heterogeneity and capacity for introgression than genetically homogeneous and reproductively conserved species. (4) Matching the target hosts susceptibility with the candidate pathogens virulence is of utmost importance for biocontrol success since host–pathogen interactions at the species and subspecies levels are often governed by single-gene differences (e.g., varietal specificity). (5) Practical and political considerations are central to the selection of targets for control with pathogens. (6) Demand from influential stakeholders for control and/or for a nonchemical or economically sustainable control typically drives the initiative as well as the continuance of biocontrol projects to their completion. (7) In the case of inundative, bioherbicide agents, the continuity and ultimate implementation of a project will be dictated by the prospects of economic returns from developing and using a pathogen. (8) The stakeholders perceptions of the effectiveness of a biocontrol program can be unpredictable, leading to conflicting views of ‘‘success.’’ In the final analysis, a good weed target for control by a pathogen is one that has strong stakeholder backing and the list of available pathogens for the target suggests a possibility of acceptable control at a cost that is competitive with those of other control options. While this conclusion is also applicable to target selection for insect biocontrol agents, it is more relevant for pathogens because of limited funding and personnel available for development of pathogens and the added cost and technological complexity of implementing bioherbicides compared to classical biocontrols. 2005 Elsevier Inc. All rights reserved.

Maternal Environment Effects on Plant Growth and Germination of Two Strains of Thlaspi arvense L.

The influence of maternal environment on plant development and seed germination of early- and late-flowering strains of Thlaspi arvense L. was studied. Compared to plants grown at 30^⚬/10^⚬C, those grown at 15^⚬/10^⚬C and 20^⚬/10^⚬C flowered more slowly, were shorter, and grew fewer leaves; seed production, however, was greatest at 20^⚬/10^⚬C. Plants of the late-flowering strain produced more leaves than those of the early-flowering strain, but there were no differences between strains in vegetative dry weight or height at harvest. On average, fresh seeds from plants of the late-flowering strain germinated at a faster rate than those from plants of the early-flowering strain. Seed dormancy increased with increasing temperature in which they developed, thus explaining some of the differences reported in the literature regarding germination of fresh seeds of T. arvense. The evolutionary implications of these results are discussed in relation to the single gene differences between the two strains.

Host–pathogen specificity in postseedling reaction of Linum usitatissimum to Melampsora lini

Eleven commercial flax cultivars and 10 race differentials, inoculated at the prebloom stage, showed significantly different levels of postseedling resistance to virulent races of flax rust. The effects of hosts and of races were significant or highly significant. Races differentiated hosts, hosts differentiated races, and host × race interaction was highly significant. Non-allelic, single-gene differences in host genotype were associated with higher levels of resistance and were ascribed to epistatic action by an L6-complex and by genes K1, M4, and N1. Epistatic action for susceptibility by gene L9 may have occurred in the race differentials Dakota (L9M) and Koto (L9P). The high aggressiveness of race 22 on 10 commercial race-differentiating hosts was correlated with possession of 26 virulence genes compared with 12–15 genes possessed by three other races. Indications are that allelism of host resistance genes and linked virulence of corresponding virulence genes, and also genetic background, were factors in host × pathogen interactions. The cultivar McGregor is a superior source of postseedling rust resistance because each of its genes K1 and L6 was associated with a high resistance level to race 22. Key words: adult plant, allelism, epistasis, flax.

Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.

Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study.

Effects of Visible Recessive Alleles on Vigor Characteristics in a Maize Hybrid1

Present knowledge of the control of heterosis and various vigor characteristics on a single gene or locus basis is inadequate. Information on this subject was obtained by producing a number of mutant recessive alleles in a maize (Zea mays L.) inbred line and selecting 31 for study. It was obvious from observation that most of the recessive alleles exhibit numerous pleiotropic effects affecting various vigor characteristics in the homozygous background of the inbred. Five of the recessive alleles were selected for this study to ascertain if pleiotropic vigor effects may also be expressed in the heterozygous background of a hybrid. Each allele produced an array of pleiotropic effects, either positive or negative, affecting various vigor characteristics in the hybrid. Considering pleiotropic effects in the context of single gene differences, the effects on individual vigor characteristics range from small to large. One allele increased the grain yield by three percent. The genetic nature of the pleiotropic effects is not clear at this time; however, it is proposed that pleiotropic effects associated with recessive alleles provide a genetic basis for heterosis.

Sympathetic nerve activity and blood pressure in normotensive backcross rats genetically related to the spontaneously hypertensive rat.

The genetic basis of hyperactivity of the sympathetic nervous system (SNA) in spontaneously hypertensive rats (SHR) was assessed by measuring SNA in animals derived from a backcross (BC) breeding program designed to isolate single gene differences causing changes in blood pressure. Selective breeding of the male hypertensive rats with inbred normotensive female Wistar/Lewis rats yielded progeny with a range of blood pressures, but whose group mean pressures were lower than the group mean pressures of the original SHR. Progressive generations had progressively lower group mean pressures. There was a positive correlation between SNA and mean arterial pressure in BC rats. These results indicate that the genetic defect in SHR may be abnormality in SNA, and the hypertension in these animals is a secondary result of this primary defect. Baroreceptor function was also assessed in SHR and in BC rats. In young (8 to 24 weeks old) SHR, baroreceptor function was similar to that in BC rats, whereas SNA was markedly increased. Only in older (24 to 40 weeks old) SHR was there an abnormality in the gain of baroreceptors. The development of hypertension in SHR therefore appears to be due to increased SNA resulting from a defect in the central nervous system. Changes in baroreceptor function are secondary to the hypertension and occur after the hypertension is established.

Inconsistency in the species concept for yeasts due to mutations during vegetative growth

The generic classification of yeasts is based mainly on morphological characteristics whereas the definition of a species depends predominantly on physiological properties such as the utilization of carbon and nitrogen sources. Classification procedures are routinely done on agar slants, and in negative tests single colonies are often noticed. These colonies are spontaneous mutations and can be idetified as such after transfer onto adequate media and appropriate genetic tests. It is sometimes possible after selection steps to obtain a completely different ‘species’. This means that in many cases the classification depends only on single gene differences, where the differences in DNA base homology is almost certainly less than 1%. Since it is rather difficult to justify a new species on the basis of a single biochemical gene mutation, it is necessary in practice to perform at regular intervals an extended series of physiological tests in order to avoid confusion in nomenclature.

Location on chromosome 1 of Rnr, a gene that regulates renin in the submaxillary gland of the mouse.

Renin activity (EC 3.4.99.19) was measured in submaxillary gland extracts from four sets of recombinant inbred mouse strains. Recombination between Rnr, a gene that mediates the susceptibility of submaxillary gland renin to induction by androgen, and Dip-1, a chromosome 1 marker, was found in only 1 of 51 recombinant inbred strains, indicating that the two genes are closely linked on chromosome 1. Renin activity in androgen-treated female mice of all recombinant inbred strains resembled that of one or the other progenitor strains, as expected if a single gene is responsible. Documentation that a single gene can have major effects on renin in the submaxillary gland of the mouse implies that single gene differences might explain known variations in renin in other species.

Evidence for cytoplasmic control of gene expression in higher plants

ONE of the difficulties of studying regulatory gene function in higher eukaryotes is the lack of genotypes with single gene differences in constant genetic backgrounds. In the Triticinae, however, the construction of a series of aneuploids1,2 makes it possible to monitor the activity of single gene loci in different genetic backgrounds. With these genotypes we have been able (unpublished results with T. Lelley) to localise the structural genes for phosphodiesterase (PDE, EC 3.1.4.1.) on chromosomes 3A, 3B and 3D of wheat, Triticum aestivum (2n=6x=42). We also showed that regulatory genes located on chromosomes 5A, 5B and 5D enhance the activity of the structural genes. We now report that extrachromosomal control of the PDE iso-enzymes is another component of this complex regulatory system.

A distribution free test for major gene differences in quantitative inheritance

In this paper a new statistical test is proposed for detecting major gene differences in quantitative inheritance. It is based on the Smirnov distribution free test and may be used to detect single gene differences between two inbred lines using data from parental, F 1, F 2 and backcross generations. An application of the test is demonstrated using data from previously published experiments on the genetic control of specific antibody production.

UV-sensitive mutants of Chlamydomonas reinhardi

Mutant strains of Chlamydomonas reinhardi have been induced by nitrosoguanidine which are highly sensitive to UV radiation. This enhanced response is due to a defective dark repair capacity. The effect of photoreactivating light is not dose-modifying in the mutants, but a comparison of the doses required to reduce the survival level to 10%, gave photoreactivating factors as large as 45 in some of the mutants, whereas in the parental wild type strain it is 4.7. By crossing mutants with each other and with the wild type, it was shown that the differences in UV response are due to single gene differences, and that several loci are involved. Two of the loci studied have been shown to influence survival in different ways—the double mutant being more sensitive than either parent.