Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Genetic background”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed2026

Single-cell RNA sequencing reveals disease associated changes in brain endothelial cells in the 5XFAD mouse.

Vascular dysfunction is a key contributor to Alzheimer’s disease (AD) pathology, where changes to the endothelium and its crucial role in maintaining blood-brain barrier (BBB) integrity have been of particular emphasis. The transgenic 5XFAD (5X Familial Alzheimer’s Disease) mouse model, which exhibits AD-related amyloidosis through FAD associated mutations in amyloid precursor protein (APP) and presenilin-1 (PS1), has become a widely adopted preclinical model in AD-related research studies. The need for cross-study standardization, accessibility, and data reproducibility has led to the widespread implementation of the C57BL/6J genetic background for maintaining this model. However, its reliability for studying vascular dysfunction and BBB alterations has been questioned due to conflicting reports in the literature. This variation is often attributed to the previously documented protective nature of the C57BL/6J background and loss of genetic background diversity. Since prior studies have mostly relied on imaging or functional assays, we herein utilized single-cell RNA sequencing (scRNAseq) to investigate AD-related molecular changes to endothelial cell populations in the 5XFAD mouse model. To initially build this resource, we focused on 12-month-old male mice, which revealed differentially expressed genes between 5XFAD and wildtype animals that mapped to signaling pathways involved in DNA damage, immune reactivity, and inflammation, among others. Many of these transcriptomic changes were zonated along the arteriovenous axis and occurred in AD genome-wide association study (GWAS) risk-associated genes. Overall, we anticipate this resource will help clarify the use of the 5XFAD model for studying AD-associated vascular changes and provide the foundation for expanded molecular profiling of brain endothelial cells under AD-associated conditions.

Animals↗
PubMed2005

Dormancy genes from weedy rice respond divergently to seed development environments.

Genes interacting with seed developmental environments control primary dormancy. To understand how a multigenic system evolved to adapt to the changing environments in weedy rice, we evaluated genetic components of three dormancy QTL in a synchronized nondormant genetic background. Two genetically identical populations segregating for qSD1, qSD7-1, and qSD12 were grown under greenhouse and natural conditions differing in temperature, relative humidity, and light intensity during seed development. Low temperatures tended to enhance dormancy in both conditions. However, genotypes responded to the environments divergently so that two populations displayed similar distributions for germination. Additive and/or dominance effects of the three loci explained approximately 90% of genetic variances and their epistases accounted for the remainder in each environment. The qSD1 and qSD7-1 main effects were increased, while the qSD12 additive effect was decreased by relatively low temperatures. Both gene main and epistatic effects were involved in G x E interactions, which in magnitude were greater than environmental main effect. The divergent responses of dormancy genes observed in this simple multigenic system presumably have selective advantages in natural populations adapted to changing environments and hence represent a genetic mechanism stabilizing the dormancy level of weedy rice ripened in different seasons or temperature regimes.

Chromosome Mapping↗
PubMedDate not supplied

Allergy as a systemic disease.

The prevalence of allergic diseases has shown an increase in the last few years. Allergic diseases develop in persons with a genetic background, this genetic trait being known as atopy. The main pathophysiological characteristic of allergy is inflammation. The inflammatory process may explain the diversity of symptoms and signs of allergy. The early sensitization increases the risk of developing different symptomatic forms of allergy, and one person may present different symptoms and signs of allergy. But some persons can become allergic without atopy trait in conditions of a higher and longer exposure to allergens (e.g. occupational allergy). In the last years new allergens have induced symptoms, sometimes with a life-threatening evolution. The load of allergen in public areas is also increasing. In this context, allergy must be understood as a unique systemic disease with various forms of presentation.

Allergens↗
PubMed2005

Role of the CCL2/MCP-1 -2518A>G gene polymorphism in HLA-B27 associated uveitis.

PURPOSE: Acute anterior uveitis (AAU) is the most common form of uveitis. Up to 50% of patients with AAU are HLA-B27 positive. Since HLA B27 itself plays only a minor role in the overall genetic background, other genetic variants are likely to contribute to the susceptibility to AAU. The chemokine (C-C motif) ligand 2 (CCL2) gene, coding for monocyte chemoattractant protein-1 (MCP-1), a chemotactic cytokine, is involved in the induction of uveitis. A CCL2 gene polymorphism, which is characterized by an A>G substitution at nucleotide -2518 in the promoter region of CCL2 has been previously shown to affect MCP-1 synthesis. The purpose of the present study was to investigate a hypothesized association between this genetic variant and the presence of HLA-B27 associated AAU. METHODS: The study group comprised 114 patients with HLA-B27 associated AAU. One hundred and eleven healthy HLA-B27 positive individuals served as the HLA-B27 positive control group, whereas 81 healthy HLA-B27 negative individuals served as a HLA-B27 negative control group. Genotyping for the CCL2 -2518A>G polymorphism was performed by polymerase chain reaction. RESULTS: Carriers of a CCL2 -2518G allele were found significantly more often in patients with HLA-B27 associated AAU than among HLA-B27 positive controls (49.2% and 31.5%, respectively; odds ratio 2.1; 95% confidence interval 1.2-3.6; p=0.007). CONCLUSIONS: Our data suggest that the CCL2 -2518A>G polymorphism may play a role in HLA-B27 associated acute anterior uveitis.

Acute Disease↗
PubMed1982

[Genetic counseling for dermatologic patients].

Many genetic and environmental influences focus on the skin, thus producing a high frequency of multifactorial diseases in this organ (genetic disposition together with exogenous force leading to manifestation) [2]. Genetic advice must be comprehensive, i.e., include aspects of diagnosis, prognosis, preventive and therapeutic management and psychological guidance of affected families. Ideally it should be given by the genetically trained dermatologist or family doctor. Pedigree analysis combined with clinical, morphological, biochemical and immunological methodology are employed to reach a diagnosis. Consideration must be given to the heterogeneity of many diseases with predominantly or partially genetic background. Here genetic analysis can help to identify clinically overlapping entities. HLA-typing contributes to identify individuals at risk in an increasing number of conditions, for instance in psoriasis. Prenatal diagnosis by fetoscopy has been accomplished in congenital ichthyosis and hereditary bullous epidermolysis. According to a rule of thumb rare conditions (monogenic, chromosomal) with a tendency to syndromic manifestation may carry a high risk of recurrence, up to over 50%, while the common diseases of multifactorial origin with usually single-organ-manifestation (here skin and/or mucous membranes) justify a more optimistical approach. Recurrence occurs in less than 10%. Disorders of fertility call for karyotype analysis in order to exclude balanced aberrations with the potential of severely malformed offspring.

Female↗
PubMed2000

The genetic structure of the Raleigh natural population of Drosophila melanogaster revisited.

The Raleigh natural population of Drosophila melanogaster was reanalyzed with special attention to possible dysgenic effects during the extraction of chromosomes. About 600 second chromosomes were extracted from the Raleigh natural population, half in the cytoplasm of wild-caught females (native genetic background) and half in the cytoplasm of the laboratory line, C160(In(2LR)SM1, Cy/In(2LR)bw(V1)) (foreign genetic background). We could not find significant differences between the two extraction schemes in the frequency of lethal second chromosomes (Q = 0.252 for the lines with the negative genetic background vs. 0.231 for the lines with the foreign genetic background) or in the homozygous detrimental (D) and lethal (L) loads (D = 0.210 vs. 0.251; L = 0.287 vs. 0.264). The effective size of the population was estimated to be approximately 19,000, based on the allelism rate of lethal-bearing chromosomes. The homozygous load markedly decreased in the 15 years since a previous study of the same population.

Animals↗
PubMed2004

Gene expression variation between mouse inbred strains.

BACKGROUND: In this study, we investigated the effect of genetic background on expression profiles. We analysed the transcriptome of mouse hindlimb muscle of five frequently used mouse inbred strains using spotted oligonucleotide microarrays. RESULTS: Through ANOVA analysis with a false discovery rate of 10%, we show that 1.4% of the analysed genes is significantly differentially expressed between these mouse strains. Differential expression of several of these genes has been confirmed by quantitative RT-PCR. The number of genes affected by genetic background is approximately ten-fold lower than the number of differentially expressed genes caused by a dystrophic genetic defect. CONCLUSIONS: We conclude that evaluation of the effect of background on gene expression profiles in the tissue under study is an effective and sensible approach when comparing expression patterns in animal models with heterogeneous genetic backgrounds. Genes affected by the genetic background can be excluded in subsequent analyses of the disease-related changes in expression profiles. This is often a more effective strategy than backcrossing and inbreeding to obtain isogenic backgrounds.

Animals↗
PubMed1992

Effect of dietary fat and cholesterol level on growing pigs selected for three generations for high or low serum cholesterol at age 56 days.

Thirty-six female pigs selected for three generations for high (HS, n = 18) and low (LS, n = 18) serum cholesterol at 56 d of age were used to test the hypothesis that the two populations would respond differently to a high-fat, high-cholesterol diet (HD) and a low-fat, low-cholesterol diet (LD). The animals were four-way crosses (Chester White x Landrace x Large White x Yorkshire). All pigs were fed a standard corn-soybean meal starter diet from weaning (at 4 wk) to 8 wk of age and a grower diet from 8 to 12 wk of age. Initial serum total cholesterol concentration at 12 wk of age was higher (P less than .05) in HS than in LS pigs (94.6 vs 76.9 mg/dL, respectively). The effect of genetic background persisted throughout the 13-wk experiment (25 wk of age); there was no interaction between diet and genetic background in serum total cholesterol (final concentrations were 114.3 mg/dL in HS-HD; 107.0 mg/dL in HS-LD; 105.9 mg/dL in LS-HD; and 89.7 mg/dL LS-LD). Trends over time revealed significant effects of diet (P less than .01) and genetic background (P less than .01) on serum total cholesterol. There was no effect of genetic background on high-density lipoprotein-cholesterol concentration; high-density lipoprotein-cholesterol as a percentage of serum total cholesterol was similar for all groups: 43% for HS-HD, 48% for HS-LD, 42% for LS-HD, and 45% for LS-LD.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed2006

The superantigen-induced polarization of T cells in rat peripheral lymph nodes is influenced by genetic polymorphisms in the IL-4 and IL-6 gene clusters.

In recent years, it has become clear that the polarization of T cells depends on the genetic background. However, due to the complexity of the genetic background of each animal, a direct comparison of the phenotype is difficult. In this study, a new rat strain LEW.BN-4-10 carrying the chromosomal regions on chromosomes 4 and 10, which harbor IL-6 and IL-4 gene clusters of BN, has been bred on the genetic background of LEW. It was asked whether these two gene clusters influence the polarization of T cell responses. As a model, the Mycoplasma arthritidis mitogen (MAM)-induced inflammation was used focusing on the microenvironment of the draining lymph node (LN). The effect of differences in these regions was tested by comparing LEW.BN-4-10 and LEW rats under steady-state conditions and upon injection of MAM into the forepaw. Under steady-state conditions, the two strains showed differences in the dendritic cell (DC) subset composition. When MAM was injected, the number of T cells in LEW.BN-4-10 rats producing T(h)2 cytokines such as IL-4 and IL-13 was significantly increased compared with LEW. The data suggest that these differences in the microenvironments in LN of LEW and LEW.BN-4-10 rats resulted in different susceptibility to the disease (increase of cells in LN and paw swelling). In addition, deviations in the distribution and function of injected effector T cells were found in the LN of LEW and LEW.BN-4-10 rats after MAM treatment. The data indicate that the IL-6 and IL-4 gene clusters are involved in polarizing T cell responses in vivo.

Animals↗
PubMed1999

The use of transgenic and mutant mice to study oxygen free radical metabolism.

To distinguish the role of Mn superoxide dismutase (MnSOD) from that of cytoplasmic CuZn superoxide dismutase (CuZnSOD), the mouse MnSOD gene (Sod2) was inactivated by homologous recombination. Sod2 -/- mice on a CD1 (outbred) genetic background die within the first 10 days of life (mean, 5.4 days) with a complex phenotype that includes dilated cardiomyopathy, accumulation of lipid in liver and skeletal muscle, metabolic acidosis and ketosis, and a severe reduction in succinate dehydrogenase (complex II) and aconitase (a TCA cycle enzyme) activities in the heart and, to a lesser extent, in other organs. These findings indicate that MnSOD is required to maintain the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide. On the other hand, Lebovitz et al. reported an independently derived MnSod null mouse (Sod2tmlLeb) on a mixed C57BL/6 and 129Sv background with a different phenotype. Because a difference in genetic background is the most likely explanation for the phenotypic differences, the two mutant lines were crossed into different genetic backgrounds for further analyses. To study the phenotype of Sod2tmlLeb mice CD1 background, the Sod2tmlLeb mice were crossed to CD1 for two generations before the -/+ mice were intercrossed to generate -/- mice. The life span distribution of CD1 < Sod2-/- > Leb was shifted to the left, indicating a shortened life span on the CD1 background. Furthermore, the CD1 < Sod2-/- > Leb mice develop metabolic acidosis at an early stage as was observed with CD1 < Sod2-/- > Cje. When Sod2tmlCje was placed on C57BL/6J (B6) background, the -/- mice were found to die either during midgestation or within the first 4 days after birth. However, when the B6 < Sod2 -/+ > Cje were crossed with DBA/2J (D2) for the generation of B6D2F2 < Sod2-/- > Cje mice, an entirely different phenotype, similar to that described by Lebovitz et al., was observed. The F2 Sod -/- mice were able to survive up to 18 days, and the animals that lived for more than 15 days displayed neurological abnormalities including ataxia and seizures. Their hearts were not as severely affected as were those of the CD1 mice, and neurological degeneration rather than heart defect appears to be the cause of death.

Animals↗
PubMed2006

Bio++: a set of C++ libraries for sequence analysis, phylogenetics, molecular evolution and population genetics.

BACKGROUND: A large number of bioinformatics applications in the fields of bio-sequence analysis, molecular evolution and population genetics typically share input/output methods, data storage requirements and data analysis algorithms. Such common features may be conveniently bundled into re-usable libraries, which enable the rapid development of new methods and robust applications. RESULTS: We present Bio++, a set of Object Oriented libraries written in C++. Available components include classes for data storage and handling (nucleotide/amino-acid/codon sequences, trees, distance matrices, population genetics datasets), various input/output formats, basic sequence manipulation (concatenation, transcription, translation, etc.), phylogenetic analysis (maximum parsimony, markov models, distance methods, likelihood computation and maximization), population genetics/genomics (diversity statistics, neutrality tests, various multi-locus analyses) and various algorithms for numerical calculus. CONCLUSION: Implementation of methods aims at being both efficient and user-friendly. A special concern was given to the library design to enable easy extension and new methods development. We defined a general hierarchy of classes that allow the developer to implement its own algorithms while remaining compatible with the rest of the libraries. Bio++ source code is distributed free of charge under the CeCILL general public licence from its website http://kimura.univ-montp2.fr/BioPP.

Algorithms↗
PubMedDate not supplied

Analysis of recombination in the centromere region of mouse chromosome 7 using ovarian teratoma and backcross methods.

Recombination near the centromere of mouse chromosome 7 was studied using data obtained from ovarian teratomas and backcrosses. The recombination percentage for the centromere-Gpi-1 (glucose phosphate isomerase-1) interval was 13.4 +/- 2.6 using the ovarian teratoma mapping method. In a backcross using the Robertsonian translocation Rb(7.18)9Lub (Rb9) as the centromeric marker, the centromere-Gpi-1 recombination percentage was 4.5 +/- 1.3, demonstrating that Rb9 suppresses recombination near the centromere of chromosome 7. The recombination percentage for the Gpi-1-Ldh-1 (lactate dehydrogenase-1) interval was estimated on the LT/Sv mouse genetic background to be 19.0 +/- 2.9 using the ovarian teratoma mapping method, a value comparable to the 15.5 +/- 4.8 reported earlier. On the same genetic background in a backcross segregating for Rb9, the Gpi-1-Ldh-1 recombination percentage was 7.1 +/- 1.6. Another backcross, without the Rb9 translocation but utilizing a different genetic background, produced a recombination percentage for the Gpi-1-Ldh-1 interval of 10.7 +/- 1.5, a value similar to that obtained in the Rb-containing cross. These results suggest that either the recombination suppression in the centromere area caused by Rb9 does not extend to the Gpi-1-Ldh-1 genetic region or, if it does, that the differing genetic backgrounds of these two crosses influence recombination. No recombinants were detected among 410 offspring produced from a backcross mating segregating for Ldh-1 and ru-2 (ruby-eye-2). Thus, the gene order of Ldh-1 and ru-2 on chromosome 7 remains uncertain.

Animals↗
PubMed2002

[Individualized tailoring of antihypertensive therapy].

Despite the publication of guidelines for the management of hypertension, there is still uncertainty among physicians regarding the right antihypertensive drug selection into the right patient. Though there have been great advances in investigating hypertension, there is only a little knowledge of the mechanisms and genetic backgrounds of 'essential hypertension'. Nationwide investigations, such as association studies dealing with a large number of patients and linkage studies using hypertensive pedigrees, are necessary to correct knowledge of individual genetic backgrounds, which influence the response to antihypertensive drug therapy. Progress toward tailoring treatment for essential hypertension and individualizing target genetic background has just started. Guidelines for the management of hypertension including the consideration of individual genetic background will be published in future days.

Antihypertensive Agents↗
PubMed1992

Genetic factors in susceptibility and resistance to experimental autoimmune uveoretinitis.

Experimental autoimmune uveoretinitis (EAU) can be induced in susceptible stains of rats and mice by immunization with purified retinal antigens, and serves as a model for human uveitis. Because strong HLA associations have been noted in a number of human uveitic diseases, we investigated the role of major histocompatibility complex (MHC) vs. non-MHC genes in the control of susceptibility to ocular autoimmunity, using the mouse and the rat EAU models. It was shown that EAU expression in mice requires both a susceptible MHC haplotype and a "permissive" genetic background. MHC control of susceptibility was tentatively mapped to the I-A subregion in H-2k. I-Ek expression appeared to have an ameliorating effect on disease. Susceptible H-2 haplotypes exhibited highest disease scores on the B10 background, and disease was reduced, or even absent, on some other (nonpermissive) backgrounds. Factors which may determine "permissiveness" or "nonpermissiveness" of a particular genetic background, as studied in mice and rats, may include diverse genetic mechanisms spanning regulation of cytokines, hormones, vascular effects and the T cell repertoire. Taken together, the data suggest that, in individuals susceptible to uveitis by virtue of their MHC, the final expression of disease will be determined by the genetic background.

Animals↗
PubMed2003

Quantitative trait symmetry independent of Hsp90 buffering: distinct modes of genetic canalization and developmental stability.

The Hsp90 chaperone buffers development against a wide range of morphological changes in many organisms and in Drosophila masks the effects of hidden genetic variation. Theory predicts that genetic and nongenetic buffering will share common mechanisms. For example, it is argued that Hsp90 genetic buffering evolved solely as a by-product of environmental buffering, and that Hsp90 should mask morphological deviations from any source. To test this idea, we examined the effect of Hsp90 on purely nongenetic variation in phenotype, measured as differences between the left and right sides of several bilaterally symmetrical bristle and wing traits in individual flies. Consistent with previous reports, Hsp90 buffered the expression of rare morphogenic variants specific to particular genetic backgrounds. However, neither trait-by-trait nor global asymmetry was affected in outbred flies treated with an Hsp90 inhibitor or across a series of inbred genetic backgrounds from a wild population tested in isogenic F1 heterozygotes carrying either (i) a dominant negative Hsp90 allele on a mutant 3rd chromosome or (ii) a null P-insertion mutation, which was introgressed into the control genetic background on all chromosomes. By contrast, Hsp90-regulated trait means and significant effects of sex, temperature, and genetic background on trait symmetry were clearly detected. We conclude that, by maintaining the function of signaling proteins, Hsp90 masks variation affecting target pathways and traits in populations independent of purely nongenetic sources of variation, refuting the idea that a single Hsp90-dependent process generally controls genetic canalization and developmental stability.

Alleles↗
PubMed1996

Identification of a developmentally regulated septin and involvement of the septins in spore formation in Saccharomyces cerevisiae.

The Saccharomyces cerevisiae CDC3, CDC10, CDC11, and CDC12 genes encode a family of related proteins, the septins, which are involved in cell division and the organization of the cell surface during vegetative growth. A search for additional S. cerevisiae septin genes using the polymerase chain reaction identified SPR3, a gene that had been identified previously on the basis of its sporulation-specific expression. The predicted SPR3 product shows 25-40% identity in amino acid sequence to the previously known septins from S. cerevisiae and other organisms. Immunoblots confirmed the sporulation-specific expression of Spr3p and showed that other septins are also present at substantial levels in sporulating cells. Consistent with the expression data, deletion of SPR3 in either of two genetic backgrounds had no detectable effect on exponentially growing cells. In one genetic background, deletion of SPR3 produced a threefold reduction in sporulation efficiency, although meiosis appeared to be completed normally. In this background, deletion of CDC10 had no detectable effect on sporulation. In the other genetic background tested, the consequences of the two deletions were reversed. Immunofluorescence observations suggest that Spr3p, Cdc3p, and Cdc11p are localized to the leading edges of the membrane sacs that form near the spindle-pole bodies and gradually extend to engulf the nuclear lobes that contain the haploid chromosome sets, thus forming the spores. Deletion of SPR3 does not prevent the localization of Cdc3p and Cdc11p, but these proteins appear to be less well organized, and the intensity of their staining is reduced. Taken together, the results suggest that the septins play important but partially redundant roles during the process of spore formation.

Amino Acid Sequence↗
PubMed2005

Quasispecies theory in the context of population genetics.

BACKGROUND: A number of recent papers have cast doubt on the applicability of the quasispecies concept to virus evolution, and have argued that population genetics is a more appropriate framework to describe virus evolution than quasispecies theory. RESULTS: I review the pertinent literature, and demonstrate for a number of cases that the quasispecies concept is equivalent to the concept of mutation-selection balance developed in population genetics, and that there is no disagreement between the population genetics of haploid, asexually-replicating organisms and quasispecies theory. CONCLUSION: Since quasispecies theory and mutation-selection balance are two sides of the same medal, the discussion about which is more appropriate to describe virus evolution is moot. In future work on virus evolution, we would do good to focus on the important questions, such as whether we can develop accurate, quantitative models of virus evolution, and to leave aside discussions about the relative merits of perfectly equivalent concepts.

Biological Evolution↗
PubMed1981

Regulation of expression of cloned bacteriophage T4 late gene 23.

The parameters governing the activity of the cloned T4 gene 23, which codes for the major T4 head protein, were analyzed. Suppressor-negative bacteria carrying wild-type T4 gene 23 cloned into plasmid pCR1 or pBR322 were infected with T4 gene 23 amber phage also carrying mutations in the following genes: (i) denA and denB (to prevent breakdown of plasmid DNA after infection) and (ii) denA, denB, and, in addition, 56 (to generate newly replicated DNA containing dCMP) and alc/unf (because mutations in this last gene allow late genes to be expressed in cytosine-containing T4 DNA). Bacteria infected with these phage were labeled with (14)C-amino acids at various times after infection, and the labeled proteins were separated by one-dimensional gel electrophoresis so that the synthesis of plasmid-coded gp23 could be compared with the synthesis of other, chromosome-coded T4 late proteins. We analyzed the effects of additional mutations that inactivate DNA replication proteins (genes 32 and 43), an RNA polymerase-binding protein (gene 55), type II topoisomerase (gene 52), and an exonuclease function involved in recombination (gene 46) on the synthesis of plasmid-coded gp23 in relation to chromosome-coded T4 late proteins. In the denA:denB:56:alc/unf genetic background, the phage chromosome-borne late genes followed the same regulatory rules (with respect to DNA replication and gp55 action) as in the denA:denB genetic background. The plasmid-carried gene 23 was also under gp55 control, but was less sensitive than the chromosomal late genes to perturbations of DNA replication. Synthesis of plasmid-coded gp23 was greatly inhibited when both the type II T4 topoisomerase and the host's DNA gyrase are inactivated. Synthesis of gp23 was also substantially affected by a mutation in gene 46, but less strongly than in the denA:denB genetic background. These observations are interpreted as follows. The plasmid-borne T4 gene 23 is primarily expressed from a late promoter. Expression of gene 23 from this late promoter responds to an activation event which involves some structural alteration of DNA. In these respects, the requirements for expressing the plasmid-borne gene 23 and chromosomal late genes are very similar (although in the denA:denB:56:alc/unf genetic background, there are significant quantitative differences). For the plasmid-borne gene 23, activation involves the T4 gp46, a protein which is required for DNA recombination. However, for the reasons presented in the accompanying paper (Jacobs et al., J. Virol. 39:31-45, 1981), we conclude that the activation of gene 23 does not require a complete breakage-reunion event which transposes that gene to a later promoter on the phage chromosome. Ways in which gp46 may actually be involved in late promoter activation on the plasmid are discussed.

Cloning, Molecular↗