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[Sex factor F of Escherichia coli K12 and its participation in mobilizing bacterial chromosomes].

The structural and functional organization of F-factor reviewed and the physical map of F DNA, supplemented with a list of genetic markers, is presented. The DNA transfer during the conjugation is considered and especial attention is given to F-gene functions involved in this process. The special sequences of F DNA, homologous to resident insertion sequences in bacterial DNA are described and its participation in plasmido-chromosomal recombinant events both dependent and independent on recA function is discussed. The mechanism for chromosome mobilization by F-Factor are reviewed. A possibility of chromosome transfer without F DNA insertion is considered. In a latter case it proposed that spontaneous single-strand breaks may serve as the origins for initiation of chromosomal transfer.

Chemical Phenomena↗
PubMed2026

Unraveling 'F' factor: towards a genetic-clinical framework for the musculoskeletal-heart crosstalk in metabolic aging.

BACKGROUND: The rising co-occurrence of cardiometabolic diseases and musculoskeletal degeneration poses a critical challenge to healthy aging, yet the shared biological mechanisms underlying this multimorbidity remain poorly defined. This study aimed to establish an integrative clinical-genetic framework to elucidate the common frailty factor, the 'F' factor, that captures the systemic vulnerability linking cardiometabolic multimorbidity (CMM) and musculoskeletal aging. METHODS: Utilizing the prospective China Health and Retirement Longitudinal Study (CHARLS) cohort, we developed and validated novel Frailty-Integrated Indices for CMM risk prediction, evaluated with machine learning models interpreted via SHapley Additive exPlanations (SHAP). Independently, we applied genomic structural equation modeling (Genomic-SEM) to integrate genome-wide association data from six traits-coronary artery disease, type 2 diabetes, hypertension, bone mineral density, frailty, and telomere length-to model a shared latent genetic factor ('F' factor). This was followed by multivariate GWAS, fine-mapping, transcriptome-wide association study (TWAS), gene-based analysis, and functional annotation to prioritize causal genes, pathways, and cell types. RESULTS: Clinically, several Frailty-Integrated Indices significantly improved CMM risk prediction, with the optimal model achieving an AUC of 0.727. Genetically, we modeled a significant shared latent genetic factor ('F' factor), pinpointing novel risk loci and implicating key genes such as APOE and SLC22A3. These genes were enriched in pathways including cellular senescence and cholesterol metabolism and showed specific expression patterns in developmental brain stages and across multi-organ endothelial cells. CONCLUSION: Our findings provide converging evidence for Musculoskeletal‑Heart crosstalk of metabolic aging and inferred the 'F' factor as a genetic correlate of a transdiagnostic state, which links genetic predisposition to metabolic dysregulation, and systemic functional decline. This work provides a multi-level biological characterization of multimorbidity liability, informing early-risk detection and preventive strategies for complex aging-related comorbidities.

Humans↗
PubMed1975

[The influence of differences in the Rec-genotype of E. coli cells on the function of sex factor F'].

Functions of the sex factor F' depended not only on damage of the genes, controlling the recombination capacity of bacterial cells, but also on suppression of the rec-gene mutations. Suppression of mutations of these genes was accompanied by the capacity of the sex factor to mobilize the chromosome for the transfer from the rec-bacterial cells. If it were demonstrated that the cells of the Jc 9604-131 strain actually carried the inverse mutation of the rec A gene, this would prove that these mutations resulted in the restoration of a recombination possibility between the sex factor F' and the bacterial chromosome.

Escherichia coli↗
PubMed1975

F-Factor-mediated restriction of bacteriophage T7: synthesis of RNA and protein in T7-infected Escherichia coli F- and F+ cells.

Bacteriophage T7 is unable to productively infect Escherichia coli strains carrying the sex factor F. T7 phage development, in terms of RNA and protein synthesis, was compared in T7-infected isogenic F- and F+ strains of E. coli. Slightly less T7 early mRNA and early protein were synthesized in F+ cells. In addition to the defect in T7 late protein production in F+ cells reported by others, significantly less T7 late mRNA was synthesized, about one-half of that produced in T7-infected F- cells. Moreover, host RNA synthesis was not completely inhibited. The protein-synthesizing ability of T7-infected F+ cells decayed much faster than that of F- cells both in vivo and in vitro. This faster decay appears to explain the failure of F+ cells to produce T7 late protein in vivo, even in the presence of a considerable amount of translatable T7 late mRNA. Therefore, it may not be necessary to postulate the involvement of specific translational discrimination against T7 late mRNA, although it appears that F-factor-mediated restriction of T7 involves changes in transcription as well as translation.

Cell-Free System↗
PubMed1979

Biochemical characterization of nonintegrated plasmid-folded chromosome complexes: sex factor F and the Escherichia coli nucleoid.

The existence of nonintegrated plasmid-chromosome complexes has been deduced in previous work from the cosedimentation of covalently closed, circular plasmids with host folded chromosomes. In the present work, it is shown that about 70 to 90% of the covalently closed, circular F deoxyribonucleic acid could be released in vitro from chromosome complexes by ribonuclease treatment but not by protease, Sarkosyl, or ethidium bromide. Consistent with the in vitro studies, Escherichia coli cells treated for 5 min with rifampin, an inhibitor of ribonucleic acid initiation, released upon lysis 90% of their plasmid deoxyribonucleic acid as freely sedimenting molecules.

Chromosomes, Bacterial↗
PubMed1975

[Properties of the F' factors formed in crosses of E. coli Hfr donor cells with recipient cells by means of defects in recombination].

Meriploids isolated from the crosses of donor cells HfrH, KL-96, KL-99 and the recipient cells AB 2463 recA carried sex factors of different structures (different in length) and activities: 1) typical F1-factors with the proximal chromosomal markers; 2) "long" F1-factors of different structures with defective genes, which controlled sensitivity to phagef2; 3) "long" F1-factors of different structures with defective genes, which controlled conjugation transfer. Chromosomal markers can be incorporated into the sex factor regardless of their position in respect to the sex factor in the initial Hfr cells. Defects of the sex factor proper in the genome are accompanied by the loss of some chromosomal genes incorporated into the sex factor. At the same time the typical F'-factors preserve their structure completely.

Bacteriophages↗
PubMed1976

Genetic and physical studies of recombinant plasmids formed between an R plasmid of compatibility group FI and sex factor F of HfrH.

Recombinant plasmids between an R plasmid of the FI group (R162/3) and the sex factor F or HfrH were produced after the conjugal transfer of this R plasmid into HfrH. Three types of recombinant plasmids were identified after the mating of HfrH (R162/3) with recA and rec+ recipients. One specimen of each type (pIP218, pIP222, pIP226) was studied in this report. All three recombinant plasmids carry the same genetic information for resistance to antibiotics (CSSuT) retained from R162/3. pIP218 retained all the other properties from F of HfrH: derepression for pilus synthesis, mobilization of the chromosome for the proximally transferred HfrH genes (thr, leu, proA), interference with T7 propagation, and ability to be cured by acridine orange. pIP222 retained from F of HfrH the derepression for pilus synthesis and the same polarity of chromosome transfer (thr, leu, proA), while pIP226 retained the interference with T7 propagation and acridine orange curing. Physical studies revealed that replication control and/or recovery of F and pIP218 as covalent circles of deoxyribonucleic acid are similar, and are different from R162/3. The new plasmids are more likely the result of a substitutive recombination event than a fusion. We propose genetic maps of these recombinant plasmids, showing the unequal participation of the parental plasmids in their formation.

Acridines↗
PubMed1979

Two Escherichia coli chromosomal cistrons, sfrA and sfrB, which are needed for expression of F factor tra functions.

Twelve mutants of Escherichia coli K-12 have been isolated which carry chromosomal mutations that exhibit pleiotropic effects on the expression of F factor tra cistrons. F pilus synthesis, deoxyribonucleic acid transfer, and surface exclusion are all inhibited. Six of the mutants carry sfrA mutations, and six carry sfrB mutations. sfrA and sfrB are cistrons mapping near thr and metE, respectively. Several F-like plasmids are dependent on sfrA and on sfrB for expression of tra cistrons. Plasmids of incompatibility groups C and S are only dependent on sfrB,and other conjugative plasmids are dependent on neither. sfrB mutations also result in changes in certain cell envelope properties, including change sensitivity to certain bacteriophages which use lipopolysaccharide as a receptor, synthesis of nonfunctional flagella, and altered sensitivity to antibiotics.

Chromosome Mapping↗
PubMed1975

F-Factor-mediated restriction of bacteriophage T7: protein synthesis in cell-free systems from T7-infected Escherichia coli F- and F+ cells.

A characteristic phenomenon in the F-factor-mediated inhibition of T7 phage is a virtual absence of T7 late protein synthesis in T7-infected Escherichia coli male cells, in spite of the presence of T7 late mRNA which is translatable in vitro when isolated from the cell. To determine whether the translational defect in T7-infected F+ cells is due to a T7 late mRNA-specific translational block, or to a general decrease of F+ cell translational activity, we compared the activities of cell-free, protein-synthesizing systems prepared from isogenic F- and F+ cells harvested at different times of T7 infection. The cell-free systems from uninfected F- and F+ cells translated T7late mRNA equally as well as MS2 RNA and T7early mRNA. The activity of cell-free systems from T7-infected F+ cells to translate MS2 RAN, T7 early mRNA, and T7 late mRNA decreased concomitantly at a much faster rate than that of T7-infected F- cells. Therefore, the abortive infection of F+ cells by T7 does not result from a T7 late mRNA-specific translational inhibition, although a general reduction of the translational activity appears to be a major factor for the inability of the F+ cells to produce a sufficient amount of T7 late proteins.

Cell-Free System↗
PubMed1978

[Determination of "settling factor" (f) by the hematopoietic stem cell cloning test in mouse spleen and bone marrow].

The effect of distribution of injected colony-forming units (CFU) in the recipient's organism was studied. The distribution was assessed by the "sedimentation factor" (f) criterion. This factor was found by the number of colonies revealed on histological sections of the spleen and femoral bone marrow in comparison with the number of colonies visible on the surface of the spleen. Macroscopic count of the colonies on the spleen permits, to assess the f value both in the whole spleen volume and in the femoral bone marrow. In this case f value was independent of the character of CFU differentiation. f value could change depending on the physiological condition of CFU population. In irradiation of the bone marrow CFU in a dose of 200, 400 and 600 R f value in the spleen decreased in comparison with control, but remained unchanged in the bone marrow.

Animals↗
PubMed1975

T7 protein synthesis in F-factor-containing cells: evidence for an episomally induced impairment of translation and relation to an alteration in membrane permeability.

T7 infection of F-factor-containing PIFA+, B+ cells is abortive. In spite of the presence of mRNA for all three classes of T7 proteins, only the earliest of the T7 proteins are synthesized. A crucial question is whether the failure of T7 to develop in PIFA+, B+ cells is the result of an inability to translate the late classes of T7 mRNA or, as has been recently suggested (Britton, and Haselkorn, 1975; Condit, 1975), whether it is the result of a more generalized alteration in membrane permeability. We have examined the effects of the wild-type PIFA+, B+ spisome and two sipsomal mutations (pifA- and pifB-) on in vitro translation and membrane permeability. In vivo the episomal mutations allow partial or complete T7 development to occur. We demonstrate that cell-free protein-synthesizing systems from T7-infected PIFA+, B+ cells show a three- to fivefold decrease in the rate of translation of both natural and synthetic mRNA. In addition, ribosomes from T7-infected PIFA+, B+ cells are defective in their ability to bind Fmet tRNAf in response to natural mRNA. By contrast, cell-free extracts from T7-infected pifA-(PIFA-, B+) celld retain the ability to bind Fmet defective T7-infected PIFA+, B+ rigosomes can be restored to full activity by a trypsin-sensitive fraction from uninfected PIFA+, B+ or T7-infected PIFA-, B+ cells. Despite the differences in translational capacity of these extracts, both T7-infected PIFA+, B+ and PIFA-, B+ cells display the same permeability lesions as measured by the loss of ATP from the cells into the supernatant. Mutation of the episome of pifB- prevents the loss of ATP from the cells after T7 infection.

Adenosine Triphosphate↗
PubMed1976

Transfer gene expression during fertility inhibition of the Escherichia coli K12 sex factor F by the I-like plasmid R62.

Further understanding of how the FinQ fertility inhibition system of the I-like plasmid R62 inhibits transfer of the sex factor F has been gained by the use of a genetic assay for individual transfer gene products. The technique involved construction of a series of Flac plasmids carrying suppressible mutations in individual transfer genes together with a FinQ inhibitor-insensitive traQ mutation. The transfer of the Flac double mutants from a strain carrying wild-type Fhis and R62 then indicated the effect of R62-encoded transfer inhibition on the expression of individual F transfer genes. During such inhibition the products of genes traJ, traA, traE, traB and traC were present in quantities sufficient to permit efficient F transfer, whereas the levels of the traF, traH, traG and traD gene products were so reduced as to limit F transfer. These findings and a failure to obtain recombination between traC and traQ mutations suggest that the R62 fertility inhibition system terminates transcription of the transfer operon between traC and traF.

Coliphages↗
PubMed1975

F factor promotes turnover of stable RNA in escherichia coli.

Male bacteria that contain and srnA- mutant allele degrade their "stable" RNA massively after RNA synthesis is blocked at 42 degrees C; a normal F- female strain shows no such RNA breakdown unless both the srnA- allele and maleness (F factor) are introduced.

Alleles↗