Historical Society of Washington, D.C. and P1 phage

The Historical Society of Washington, D.C. (named The Columbia Historical Society until 1988) is an educational foundation and museum dedicated to preserving and displaying the history of Washington, D.C. The society provides lectures, exhibits, classes, community events, and other educational programs as part of its mission. In addition, the society's Kiplinger Research Library houses a collection of books, maps, photographs, and other materials relevant to the history of the city.

Located in the center of Mount Vernon Square in Washington, the society occupies a Beaux-Arts building funded by Andrew Carnegie in 1902 (one of his many Carnegie libraries), originally used as the District of Columbia Public Library. The former library building is open to the public from Monday through Sunday 10am to 5pm. Visitors are welcome to tour current exhibits and use the society's library.

Contents 1 History 1.1 City Museum of Washington, D.C. 1.2 Recent history 2 References 3 External links


The Columbia Historical Society, as it was called until 1988, was founded in 1894 by a group of 36 men and women, with the following mission: "Its objects shall be the collection, preservation, and diffusion of knowledge respecting the history and topography of the District of Columbia and national history and biography." The organization had as its goal "collecting the scattered and rapidly disappearing records of events and individuals prominent in the history of the city and District." The main role of the early Society was to serve as a forum for members to present historical research, which was then published in the Records of the Columbia Historical Society. It was also a collecting organization, amassing library and manuscript collections.

By 1899 the new organization had 108 members, all but 13 of whom were men, and all but seven of whom were residents of Northwest Washington. Although African Americans constituted one-third of the then-racially segregated city's population, the membership of the Columbia Historical Society was all white. Membership dues went largely to support the publication of the Records. These hard-bound volumes appeared every year until 1922, and thereafter every two or three years.

The growing collections began to present difficulties almost immediately. For more than 50 years, the Society used rented and donated rooms to house its offices and library. Volunteers served as librarians and curators. In the late 1940s, a bill to finance reassembly of Francis Scott Key's home and give it to the Society passed Congress, but President Harry Truman vetoed it for budgetary reasons. A professional appointed in 1947 promulgated a collecting policy and created the first catalog.

In 1954, the District of Columbia Public Library, which had been storing the Society's collections, threatened eviction because of its own space problems. The Society's Board of Trustees appealed to the membership for a home. In 1955, Amelia Keyser Heurich, widow of prominent Washington brewer Christian Heurich (see: Heurich Brewery), donated the family's four-story mansion (see: Christian Heurich Mansion) near Dupont Circle, which became the Society’s headquarters. The Society took possession of the mansion during the following year when Mrs. Heurich died.

The Society hired its first director in 1959, although the office of the Board of Trustees' president, Ulysses S. Grant III, who served from 1952 to 1968, performed most of the Society's work. For many years the house chairman lived on the third floor and rented offices in the building to other historical and patriotic organizations. Space was available for a library in the mansion, which housed the book, manuscript, photograph and other collections.

In 1975, a real estate transaction produced a significant endowment, which was used to hire the first full-time, professional historian as executive director, Perry Fisher. Fisher used the renewed interest in the nation's past stimulated by the U.S. Bicentennial to increase the Society's services to the general public as well as its membership.

The programs and reach of the Society continued to expand. In 1989 the Society announced its new name: The Historical Society of Washington, D.C. The Society announced the name change with the first issue of Washington History, a semi-annual magazine that continued the publishing traditions of the Records in a new format. City Museum of Washington, D.C.

In 1998, Monica Scott Beckham, Vice President of the Society's Board of Trustees, went before a subcommittee of the U.S. House of Representatives Committee on Appropriations to seek federal funding for a City Museum of Washington, D.C. Congress appropriated $2,000,000 in 1999 "provided that the District of Columbia shall lease the Carnegie Library at Mount Vernon Square to the Society . . . for 99 years at $1 per year . . .". On July 14, 1999, District Mayor Anthony A. Williams announced the creation of the City Museum of Washington, D.C. in the Carnegie Library.

The City Museum opened in May 2003. However, the Museum closed in November 2004 because of a lack of funding and interest. Recent history Carnegie Library in 2012.

In 2006, the Society and the National Music Center entered into an agreement that permitted the Music Center to occupy a substantial portion of the Carnegie Library for the next three years.

The Carnegie Library now houses the Society’s research library, rotating exhibits, and offices. Ninety percent of the Society’s historic collections, which include artworks, documents, maps, objects, and over 100,000 photographs, are stored on-site. A permanent exhibition, Window to Washington, now traces the development of the District’s built environment and serves as an introduction to the Society’s collections. The Society also provides research workshops to students and community groups, including D.C. Public Charter Schools and universities.

P1 phage and Historical Society of Washington, D.C.

P1 is a temperate bacteriophage (phage) that infects Escherichia coli and a some other bacteria. When undergoing a lysogenic cycle the phage genome exists as a plasmid in the bacterium unlike other phages (e.g. the lambda phage) that integrate into the host DNA. * P1 has an icosahedral "head" containing the DNA attached to a contractile tail with six tail fibers. The P1 phage has gained research interest because it can be used to transduce the phenotype of a target bacterium. As it replicates during its lytic cycle it captures fragments of the host chromosome. If the resulting viral particles are used to infect a different host the captured dna fragments can be integrated into the new host's genome. This method of in vivo genetic engineering was widely used for many years and is still used today, though to a lesser extent. P1 can also be used to create the P1-derived artificial chromosome cloning vector which can carry relatively large fragments of DNA. Also, P1 encodes a site-specific recombinase, Cre, that is widely used to carry out cell-specific or time-specific DNA recombination by flanking the target DNA with loxP sites.(see Cre-Lox recombination)

Contents 1 Morphology 2 Genome 3 Life cycle 3.1 Infection and early stages 3.2 Lysogeny 3.3 Lysis 4 References 5 External links


The virion is similar in structure to the T4 phage but simpler. It has an icosahedral head containing the genome attached at one vertex to the tail. The tail has a tube surrounded by a contractile sheath. It ends in a base plate with six tail fibres. The tail fibres are involved in attaching to the host and providing specificity. Genome

The genome of the P1 phage is moderately large, around 93Kbp in length (compared to the genomes of e.g. T4 - 169Kbp, lambda - 48Kbp and Ff - 6.4Kbp). In the viral particle it is in the form of a linear double stranded DNA molecule. Once inserted into the host it circularizes and replicates as a plasmid.

In the viral particle the DNA molecule is longer (110Kbp) than the actual length of the genome. It is created by cutting an appropriately sized fragment from a concatemeric DNA chain having multiple copies of the genome. (see the section below on lysis for how this is made) Due to this the ends of the DNA molecule are identical. This is referred to as being "terminally redundant". This is important for the DNA to be circularized in the host. Another consequence of the DNA being cut out of a concatemer is that a given linear molecule can start at any location on the circular genome. This is called a cyclical permutation.

The genome is especially rich in Chi sequences recognized by the bacterial recombinase RecBCD. The genome contains two origins of replication, oriR which replicates it during the lysogenic cycle and oriL which replicates it during the lytic stage. The genome of P1 has 112 protein coding and 5 untranslated genes. It even encodes 3 of its own tRNAs which are expressed in the lytic stage.

The gene that encodes the tail fibers have an set of sequences that can be targeted by a site specific recombinase Cin. This causes the C terminal end of the protein to switch between two alternate forms at a low frequency. The viral tail fibers are responsible for the specificity of binding to the host receptor. The targets of the viral tail fibers are under a constant pressure to evolve and evade binding. This method of recombinational diversity of the tail allows the virus to keep up with the bacterium. This system has close sequence homologies to recombinational systems in the tail fibers of unrelated phages like the mu phage and the lambda phage. Life cycle

Temperate phage, such as P1, have the ability to exist within the bacterial cell they infect in two different ways. In lysogeny, * See note added above about the errors in the preceding and following sentences. P1 can exist within a bacterial cell as a circular DNA in that it exists by replicating as if it were a plasmid and does not cause cell death. Alternatively, in its lytic phase, P1 can promote cell lysis during growth resulting in host cell death. During lysogeny new phage particles are not produced. In contrast, during lytic growth many new phage particles are assembled and released from the cell. By alternating between these two modes of infection, P1 can survive during extreme nutritional conditions that may be imposed upon the bacterial host in which it exists.

A unique feature of phage P1 is that during lysogeny its genome is not incorporated into the bacterial chromosome as is commonly observed during lysogeny of other bacteriophage. Instead, P1 exists independently within the bacterial cell, much like a plasmid would. P1 replicates as a 90 kilobase (kb) plasmid in the lysogenic state and is partitioned equally into two new daughter cells during normal cell division. Infection and early stages

The phage particle adsorbs onto the surface of the bacterium using the tail fibers for specificity. The tail sheath contracts and the DNA of the phage is injected into the host cell. The host DNA recombination machinery or the cre enzyme translated from the viral DNA recombine the terminally redundant ends and circularize the genome. Depending on various physiological cues, the phage may immediately proceed to the lytic phase or it may enter a lysogenic state. Lysogeny

The genome of the P1 phage is maintained as a low copy number plasmid in the bacterium. The relatively large size of the plasmid requires it to keep a low copy number lest it become too large a metabolic burden while it is a lysogen. As there is usually only one copy of the plasmid per bacterial genome, the plasmid stands a high chance of not being passed to both daughter cells. The P1 plasmid combats this by several methods: The plasmid replication is tightly regulated by a RepA protein dependent mechanism. This is similar to the mechanism used by several other plasmids. It ensure that the plasmid divides in step with the host genome. Interlocked plasmids are quickly unlinked by Cre-lox recombination The plasmid encodes a plasmid addiction system that kills daughter cells that lose the plasmid. It consists of a stable protein toxin and an antitoxin that reversibly binds to and neutralizes it. Cells that lose the plasmid get killed as the antitoxin gets degraded faster than the toxin. Lysis

The P1 plasmid has a separate origin of replication (oriL) that is activated during the lytic cycle. Replication begins by a regular bidirectional theta replication at oriL but later in the lytic phase,it switches to a rolling circle method of replication using the host recombination machinery. This results in numerous copies of the genome being present on a single linear DNA molecule called a concatemer. The end of the concatemer is cut a specific site called the pac site or packaging site. This is followed by the packing of the DNA into the heads till they are full. The rest of the concatemer that does not fit into one head is separated and the machinery begins packing this into a new head. The location of the cut is not sequence specific. Each head holds around 110kbp of DNA so there is a little more than one complete copy of the genome (~90kbp) in each head, with the ends of the strand in each head being identical. After infecting a new cell this "terminal redundancy" is used by the host recombination machinery to cyclize the genome if it lacks two copies of the lox locus. If two lox sites are present (one in each terminally redundant end) the cyclization is carried out by the cre recombinase.

Once the complete virions are assembled, the host cell is lysed, releasing the viral particles.
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