Fertility factor

The Fertility factor (first named F by its discoverer Esther Lederberg) was the first episome discovered (viral DNA that is separate from bacterial DNA). "F" is often confused with sexual conjugation. Sexual conjugation is a bacterial DNA sequence that allows a bacterium to produce a sex pilus necessary for conjugation. A common form of F factor is an F plasmid. Unlike other plasmids, F factor is constitutive for transfer proteins due to the gene traJ. The F plasmid belongs to a class of conjugative plasmids that control sexual functions of bacteria with a fertility inhibition (Fin) system.

The fertility factor "F" also participates in Transduction. Generalized transduction was discovered by Norton Zinder, who published his results with Esther Lederberg, Joshua Lederberg and Evelyn Lively.[1]

Contents

Discovery of Fertility factor "F"

Esther M. Lederberg discovered "F" working alone[2], subsequently publishing (as principal investigator) with Joshua Lederberg and Luigi L. Cavalli-Sforza.[3] Once her results were announced, two other labs joined the studies. "This was not a simultaneous independent discovery of F (I names as Fertility Factor until it was understood.) We wrote to Hayes, Jacob, & Wollman who then proceeded with their studies."[4] The discovery of "F" has sometimes been confused with William Hayes' discovery of "sex factor", though he never claimed priority. Indeed, "he [Hayes] thought F was really lambda, and when we convinced him [that it was not], he then began his work."[5]

Corroboration by Luigi L. Cavalli-Sforza that Esther Lederberg had priority in discovering the fertility factor F (the first episome) can be found at http://www.estherlederberg.com/Clark_MemorialVita/LLCS%20Cavalli-testimonial15.html.[6]

Structure

The most common functional segments constituting F factors are:

Some F plasmid genes and their Function Genes Function traA Pilin, Major subunit of the pilus.

Relation to the genome

The F factor is an episome and can exist as an independent plasmid or integrate into the bacterial cell's genome. There are several names for the possible states:

Function

When an F+ cell conjugates/mates with an F cell, the result is two F+ cells, both capable of transmitting the plasmid further by conjugation. The F-plasmid belongs to a class of conjugative plasmids that control sexual functions of bacteria with a fertility inhibition (Fin) system. In this system, a trans-acting factor, FinO, and antisense RNAs, FinP, combine to repress the expression of the activator gene TraJ. TraJ is a transcription factor that upregulates the tra operon. The tra operon includes genes required for conjugation and plasmid transfer. This means that an F+ bacteria can always act as a donor cell. The finO gene of the original F plasmid is interrupted by an IS3 insertion, resulting in constitutive tra operon expression, in E. coli K12.[7][8] F+ cells also have the surface exclusion proteins TraS and TraT on the bacterial surface. These proteins prevent secondary mating events involving plasmids belonging to the same incompatibility (Inc) group. Thus, each F+ bacterium can host only a single plasmid type of any given incompatibility group.

In the case of Hfr transfer, the resulting transconjugates are Hfr cells as well. When F-prime plasmids are transferred to a recipient bacterial cell, they carry pieces of the donor's DNA that can become important in recombination. Bioengineers have created F plasmids that can contain inserted foreign DNA; this is called a bacterial artificial chromosome.

The first DNA helicase ever described is encoded on the F-plasmid and is responsible for initiating plasmid transfer. It was originally called E. coli DNA Helicase I, but is now known as F-plasmid TraI. In addition to being a helicase, the 1756 amino acid (one of the largest in E. coli) F-plasmid TraI protein is also responsible for both specific and non-specific single-stranded DNA binding as well as catalyzing the nicking of single-stranded DNA at the origin of transfer.

See also

References

  1. ^ Lederberg, J., Lederberg, E. M., Zinder, N. D., Lively, E. R., 1951, "Recombination analysis of bacterial heredity", Cold Spring Harbor Symposia on Quantitative Biology 16:413-443
  2. ^ "The initial experiments were designed to explain an unexpected observation. There were no 'people', just myself, and discussions with J.L." See http://www.estherMlederberg.com/Clark_MemorialVita/HISTORY52.html
  3. ^ Lederberg, J., Cavalli, L. L., and Lederberg, E. M., Nov. 1952, "Sex compatibility in Escherichia coli", Genetics 37(6):720-730
  4. ^ http://www.estherMlederberg.com/Clark_MemorialVita/Eric%202%20FFactor5.html
  5. ^ http://www.estherMlederberg.com/Clark_MemorialVita/Eric%201%20FFactor5.html
  6. ^ For a detailed discussion, see http://www.estherlederberg.com/Censorship/CensorshipIndex.html; click "Fertility Factor F".
  7. ^ Jerome, LJ; van Biesen T, Frost LS (1999). "Degradation of FinP antisense RNA from F-like plasmids: the RNA-binding protein, FinO, protects FinP from ribonuclease E". J Mol Biol 285 (4): 1457–1473. doi:10.1006/jmbi.1998.2404. PMID 9917389. 
  8. ^ Arthur DC, Ghetu AF, Gubbins MJ, Edwards RA, Frost LS, Glover JN (2003). "FinO is an RNA chaperone that facilitates sense-antisense RNA interactions". EMBO J. 22 (23): 6346–55. doi:10.1093/emboj/cdg607. PMC 291848. PMID 14633993. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=291848. 

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