Bacteriophage Diagram: Labeled 3D T4 Phage, Parts and Life Cycle

A bacteriophage (phage) is a virus that infects bacteria. The best-known phage, T4, has an icosahedral head made of protein that holds its double-stranded DNA, a neck and collar with six whiskers, a tail made of a hollow tube inside a contractile sheath, a hexagonal baseplate, and twelve tail fibres: six long and six short. Those are the parts labeled on almost every bacteriophage diagram.

"Bacteriophage" means "bacteria eater". Phages have no cell, no ribosomes and no metabolism of their own. Outside a host they are inert particles; inside one, they take over the cell's machinery to make copies of themselves. NCERT describes viruses in just these terms: non-cellular, inert outside a living cell, and obligate parasites, with bacteriophages usually being double-stranded DNA viruses. (NCERT Biology Class XI, Chapter 2.)

This page uses Enterobacteria phage T4 as the reference virus. T4 infects Escherichia coli and is one of the most studied biological objects on Earth; its structure has been solved almost atom by atom with cryo-electron microscopy and X-ray crystallography. Where other phages differ, the text says so. For viruses of plants and animals, see the virus structure page, and for the host cell itself, the bacterial cell diagram.

A labeled diagram of bacteriophage T4 shows, from top to bottom: the head (capsid) with the DNA inside and the portal at its lower corner; the neck, ringed by the collar and its whiskers; the contractile sheath around the tail tube; and the baseplate, from which the short tail fibres, the central needle and six kinked long tail fibres hang.

School diagrams often use simpler labels. The NCERT Class 11 figure of a bacteriophage, for example, labels just the head, collar, sheath and tail fibres; some older diagrams add the base plate and tail pins (an old name for the short fibres and spikes under the baseplate). In the 3D model, switch on All labels to see every part at once. (NCERT Biology Class XI, Figure 2.6.)

Each part of a bacteriophage has a job in one of two tasks: protecting the genome outside the cell, or finding a host and getting the genome into it. The table covers every part a school or university diagram asks for.

This is the text version of the 3D model: every labeled structure, grouped by region, with what it does. The E. coli envelope parts are included because they are what the phage interacts with. Use the list as a study sheet or to check a labeling worksheet.

Phage T4 is about 250 nm from the top of its head to the bottom of its baseplate, with a 120 nm × 86 nm head and a tail about 130 nm long including the baseplate. These measurements come from cryo-electron microscopy and crystal structures; each row gives its source.

Two measurements differ between sources. Leiman et al. give the hexagonal baseplate as about 52 nm and the star as 61 nm across, while Hu et al. describe the change as a widening from about 40 to 60 nm. Rao and Black give the genome as 171 kb in places, while the reference sequence is 168,903 bp; ViralZone rounds it to about 169 kb. (Leiman et al. (2010): Morphogenesis of the T4 tail and tail fibers, Virology Journal; Hu, Margolin, Molineux & Liu (2015): Structural remodeling of bacteriophage T4 and host membranes during infection initiation, PNAS; ViralZone: Tequatrovirus (T4).)

A T4 phage infects E. coli in five steps: its long tail fibres bind receptors on the cell surface, the baseplate changes shape and the short tail fibres lock on, the sheath contracts and drives the tail tube through the outer membrane, the needle's lysozyme opens the cell wall, and the DNA passes through the tube into the cytoplasm. Step through it below, and compare the two states of the 3D model above.

Adsorption (attachment). The tip of each long tail fibre, gp37, recognises the outer-membrane porin OmpC on E. coli K-12, or the glucosyl-α-1,3-glucose end of rough lipopolysaccharide (LPS) on E. coli B. A phage needs at least three long fibres to be infectious. This first binding is reversible. (Leiman et al. 2010.)

Irreversible binding. When the baseplate changes from hexagon to star, the short tail fibres swing down and bind the innermost part of LPS. Miller et al. place this second receptor at the heptose of the LPS inner core; Hu et al. describe it as the lipid A–KDO region. Either way, the phage is now anchored. (Miller et al. (2003): Bacteriophage T4 genome, Microbiology and Molecular Biology Reviews; Hu, Margolin, Molineux & Liu (2015): Structural remodeling of bacteriophage T4 and host membranes during infection initiation, PNAS.)

Sheath contraction and DNA injection. The sheath fires, the tube crosses the outer membrane, and gp5's lysozyme digests the peptidoglycan. Cryo-electron tomograms show that the tube tip stops about 24 nm into the periplasm and the inner membrane bulges out by about 16 nm to fuse with it. Fusion does not need energy from the cell, but moving the DNA across does: it needs the proton motive force of the inner membrane. (Hu et al. 2015.)

The T4 tail sheath is a spring-loaded protein tube: extended, it is 92.5 nm long and 24 nm wide; contracted, it is 42 nm long and 33 nm wide. The extended sheath, like the hexagonal baseplate, is a high-energy, metastable assembly: once triggered, its 138 subunits slide into a tighter packing with about four times more contact between them, releasing the stored energy in one go. A phage can fire only once.

• Contractile tail sheath (gp18): When the baseplate is triggered, the sheath snaps into a shorter, fatter form (42 nm long, 33 nm wide), driving the inner tube through the host's outer membrane like a syringe.
• Tail tube (gp19): The 'needle' through which the DNA travels from the head into the bacterium.
• Baseplate: The phage's trigger. When the tail fibres bind the host, the baseplate opens from a hexagon into a flat star (61 nm across, 12 nm thick), which releases the short tail fibres and sets off sheath contraction.
• Central hub and needle (gp27, gp5): Punctures the outer membrane, then the lysozyme part of gp5 digests a small hole in the peptidoglycan cell wall so the tube can pass.

The same kind of contractile tail is used by many tailed phages, and bacteria have borrowed it: the type VI secretion system that some bacteria use to inject toxins into neighbouring cells appears to be related to a phage tail. (Leiman et al. 2010.)

Bacteriophages reproduce by one of two life cycles. In the lytic cycle the phage multiplies at once and bursts (lyses) the cell to release new phages. In the lysogenic cycle a temperate phage inserts its genome into the host chromosome as a prophage and is passed on quietly when the cell divides, until it is induced to switch to the lytic cycle. (OpenStax Microbiology 6.2.)

The lytic cycle of T4 has five stages: attachment, penetration, biosynthesis, maturation and release. T4 is a virulent phage: it can only follow the lytic cycle, and every infected cell dies.

1. Attachment. The tail fibres bind specific receptors on the cell surface (OmpC or LPS for T4). Because receptors differ between bacteria, most phages have a narrow host range.
2. Penetration. The sheath contracts and the DNA is injected through the tail tube, which acts like a hypodermic needle. The empty protein coat stays outside.
3. Biosynthesis. Phage genes are switched on in three waves (early, middle and late). Early proteins shut down host gene expression and break down the host chromosome; the cytosine-free T4 DNA, made with 5-hydroxymethylcytosine, is protected. The phage DNA is then copied many times, and late genes make the head, tail and fibre proteins.
4. Maturation (assembly). Heads, tails and fibres are built on separate assembly lines. Each empty head is filled with DNA by the packaging motor at the portal; then the tail joins at the neck and the fibres are added last.
5. Release. A phage holin (gene t) makes holes in the inner membrane at a set time, letting the phage endolysin (T4 lysozyme, gene e) reach and digest the peptidoglycan wall. The cell bursts and the new phages escape. Without either protein, lysis does not happen.

(OpenStax Microbiology, 6.2 The viral life cycle; Miller et al. (2003): Bacteriophage T4 genome, Microbiology and Molecular Biology Reviews.)

The number of phages released from one cell is the burst size. Classic measurements for the T phages give bursts of roughly 120 to 300 per cell. (BioNumbers BNID 105870.) T-even phages can also delay lysis when many other phages are around (lysis inhibition), making more phages from each cell while hosts are scarce. (Miller et al. 2003.)

In the lysogenic cycle a temperate phage such as lambda (λ) joins its DNA to the host chromosome instead of killing the cell. The integrated phage genome is called a prophage, and a bacterium carrying one is a lysogen. The prophage is copied along with the host chromosome every time the cell divides. (OpenStax Microbiology 6.2.)

• Entry. Lambda binds LamB, an outer-membrane porin used for maltose uptake, and injects its 48,502 bp genome through its long, flexible tail. The genome circularises by its 12-base sticky ends (cos sites).
• The decision. The phage protein CII tips the cell towards lysogeny; the competing regulator Cro favours the lytic cycle.
• Integration. The phage enzyme integrase (Int) joins the phage circle to the chromosome by site-specific recombination.
• Staying quiet. The CI repressor keeps the lytic genes switched off, so the lysogen grows normally.
• Induction. When the host DNA is damaged, for example by ultraviolet light, the host protein RecA is activated by single-stranded DNA. Activated RecA makes CI cut itself, the repressor falls away, Int and Xis cut the prophage out (excision), and the phage enters the lytic cycle.
• Release. Lambda lyses the cell with three kinds of protein: the holin S105 makes large holes in the inner membrane, the endolysin R digests the cell wall, and the spanins Rz and Rz1 break the outer membrane.

(Casjens & Hendrix 2015.)

A prophage can change the bacterium it lives in, which is called phage conversion. The genes for the cholera toxin of Vibrio cholerae and the botulinum toxin of Clostridium botulinum are carried by phages. Phages can also move bacterial genes between cells: in generalized transduction a random piece of host DNA is packed into a phage head during the lytic cycle, and in specialized transduction an excising prophage takes neighbouring host genes with it. (OpenStax Microbiology 6.2.)

Bacteriophages come in several shapes. The best-known phages are tailed phages with an icosahedral head and double-stranded DNA; their tails can be contractile (T4), long and flexible (lambda) or short (T7). Others have no tail at all: filamentous phages such as M13 are long protein rods, and small RNA phages such as MS2 are tiny icosahedra.

(ViralZone: Tequatrovirus (T4); ViralZone: Lambdavirus; ViralZone: Teseptimavirus (T7); ICTV Report: family Inoviridae (M13); ViralZone: Emesvirus (MS2).)

Filamentous bacteriophage. An M13 particle is a helical tube of about 2,700 copies of the major coat protein p8 around a single-stranded DNA circle, plus five copies each of four minor coat proteins (p3, p6, p7 and p9). The p3 protein at one end binds the tip of a pilus, which retracts and brings the phage to the TolQRA entry receptor. New particles are pushed out through the membrane while the cell keeps growing, so M13 causes a chronic infection rather than lysis. This is why filamentous phages became the workhorse of phage display. (ICTV: Inoviridae.)

Older textbooks classify tailed phages into three families by tail shape: Myoviridae (contractile tail, like T4), Siphoviridae (long, flexible tail, like lambda) and Podoviridae (short tail, like T7), all in the order Caudovirales. In 2022 the International Committee on Taxonomy of Viruses (ICTV) abolished all three families and the order. (Turner et al. 2023.)

The reason is evolution. Genome comparisons showed that each of the old families was polyphyletic: phages with similar tails did not share one common ancestor, so grouping them by shape did not reflect their history. All tailed phages with an icosahedral head and dsDNA genome now sit in the class Caudoviricetes, divided into families defined by shared genes. The T4-like phages are in the family Straboviridae, and the species once called Escherichia virus T4 is now Tequatrovirus T4 (genus Tequatrovirus, subfamily Tevenvirinae). The same update brought in two-part (binomial) species names.

The words myovirus, siphovirus and podovirus are still fine to use as plain descriptions of a phage's shape. The ICTV says they can be used freely, but no longer have any formal taxonomic meaning. Exam syllabi may still use the old family names, so it is worth knowing both. (Turner et al. 2023.)

The T-even phages are T2, T4 and T6, three closely related E. coli phages with the same head, contractile tail and fibres. The name comes from the 1940s, when phage researchers agreed to work on one standard set of seven phages that all grow on E. coli B, numbered T1 to T7 ("T" for type). The even-numbered ones turned out to be one family, distinct from the "T-odd" phages such as T7. (BioNumbers BNID 106725.)

A T2 diagram therefore looks almost exactly like a T4 diagram: the same prolate head, collar, contractile sheath, baseplate and fibres. T2 is the phage used in the Hershey–Chase experiment, and T4 became the main model for phage structure and genetics.

Phage therapy is the use of lytic bacteriophages to treat bacterial infections. A phage attacks only the bacteria it can bind, so a well-chosen phage kills the pathogen without harming human cells or most of the normal microbiota, and it multiplies where its host is. (Gordillo Altamirano & Barr 2019.)

Félix d'Hérelle coined the word "bacteriophage" and began treating patients with phages in the early twentieth century. Enthusiasm faded in the West in the 1940s, when antibiotics arrived and reviews criticised early studies for weak methods, but the work continued, notably at the Eliava Institute in Tbilisi, Georgia (founded 1923) and the Hirszfeld Institute in Wrocław, Poland (founded 1952). (Gordillo Altamirano & Barr 2019.)

Rising antibiotic resistance has brought phages back. In a widely reported 2017 case in the United States, a 68-year-old man with a multidrug-resistant Acinetobacter baumannii infection improved after receiving phage cocktails matched to his strain. Treatments today are usually personalised: the patient's bacterium is isolated, phages that kill it are chosen from a library, and they are often given together with antibiotics, which can work in synergy. The main hurdles are the need to identify the exact bacterium, bacteria evolving resistance to the phage, the immune response, and the lack of a regulatory framework designed for living, evolving medicines. (Gordillo Altamirano & Barr 2019.)

Bacteriophages are tools as well as viruses. Two uses appear in almost every biology course: the Hershey–Chase experiment, which showed that genes are made of DNA, and phage display, which won a share of the 2018 Nobel Prize in Chemistry.

The Hershey–Chase experiment

In 1952 Alfred Hershey and Martha Chase grew phage T2 with radioactive sulfur (³⁵S), which labels protein, or radioactive phosphorus (³²P), which labels DNA. They let each batch infect E. coli, shook the cells in a kitchen blender to knock off the phage coats, and spun the mixture in a centrifuge. The ³⁵S stayed in the liquid with the empty coats, while the ³²P went into the pellet of infected cells. So the part of the phage that enters the cell and directs the making of new phages is the DNA. (OpenStax Biology 2e 14.1.)

The original paper was more cautious than textbook summaries. Blending removed about 75% of the phage sulfur but only about 15% of the phosphorus, and the authors concluded that the protein "probably has no function in the growth of intracellular phage" and that "the DNA has some function". Even so, the experiment quickly became the classic evidence that DNA, not protein, is the genetic material. (Hershey & Chase 1952.)

Phage display

In phage display, a gene for a foreign peptide or protein is joined to the gene for a phage coat protein, so the new protein is displayed on the outside of the phage while its gene is carried inside. A library of billions of such phages can be washed over a target molecule; the phages that stick are kept, multiplied in bacteria, and selected again. George Smith developed the method in 1985 with filamentous phages, and Gregory Winter used it to evolve antibodies for medicine. The first drug made this way, adalimumab, was approved in 2002 for rheumatoid arthritis, psoriasis and inflammatory bowel diseases. Smith and Winter shared half of the 2018 Nobel Prize in Chemistry "for the phage display of peptides and antibodies". (Nobel Prize in Chemistry 2018.)

T4 is used for display too: its Hoc and Soc head proteins can be fused to pieces of other proteins, and have been used to display antigens from HIV, Bacillus anthracis and foot-and-mouth disease virus for vaccine research. (Rao & Black 2010.)

For Class 8 and 9 science, a bacteriophage is simply a virus that infects bacteria. Viruses are microscopic, smaller than bacteria, and can only reproduce inside the cells of a host, which may be a bacterium, a plant or an animal. (NCERT Science Class VIII, Chapter 2.)

• Head: a protein box (capsid) with many sides. It holds the genetic material, DNA.
• Collar: the narrow ring that joins the head to the tail.
• Tail (sheath): a hollow tube that works like an injection syringe.
• Base plate: the flat plate at the end of the tail.
• Tail fibres: thin "legs" that hold on to the bacterium.

How it multiplies: the phage sits on a bacterium with its tail fibres, injects its DNA through the tail, and leaves its protein coat outside. The DNA makes the bacterium build many new phages. Then the bacterium bursts open and the new phages are released to infect other bacteria.

Is it living? Outside a cell a virus does nothing at all and can even be crystallised. Inside a cell it reproduces. That is why viruses are said to lie on the border between living and non-living things. A virus has either DNA or RNA, never both; bacteriophages usually have double-stranded DNA. (NCERT Biology Class XI, Chapter 2.)

Drawing tip for exams: draw a six-sided head on top, a short collar, a long rectangular tail with horizontal lines for the sheath, a flat base plate, and six bent tail fibres spreading out below. Label head, DNA, collar, sheath, base plate and tail fibres.

Test yourself on the parts of a bacteriophage. Write the name of each numbered part, then check your answers below. Numbers run down the left side first, then down the right.

Short-answer questions: (1) Which part of the phage enters the bacterium? Only the DNA (and a few internal proteins); the coat stays outside. (2) What makes the tail contract? The baseplate changes from a hexagon to a star after the tail fibres bind the host. (3) Name the two proteins that burst the cell at the end of the lytic cycle. Holin and endolysin (T4 lysozyme). (4) What is a prophage? Phage DNA integrated into the bacterial chromosome during the lysogenic cycle.

The T4 baseplate is a spring-loaded trap. In the free phage it is held in a high-energy, 'metastable' hexagonal shape, and the sheath above it is held stretched. The trigger is mechanical. When a long tail fibre binds the host, the fibre swings like a lever, moving the gp9 socket and the gp11 trimer it is attached to. Each gp11–gp10 unit then rotates by about 100°, which loosens the garland of short tail fibres and lets the whole baseplate unlock into its low-energy star shape. (Leiman et al. (2010): Morphogenesis of the T4 tail and tail fibers, Virology Journal.)

Because the long and short fibres compete for the same binding site on gp11, only one kind can be locked in place at a time. That makes the switch all-or-nothing: either the baseplate stays hexagonal, or it opens fully and fires the sheath. The same kind of machine turns up outside phages: the type VI secretion system, found in at least a quarter of Gram-negative bacteria, appears to be related to a phage tail. (Leiman et al. (2010): Morphogenesis of the T4 tail and tail fibers, Virology Journal.)

Cryo-electron tomography of real infections added a twist to the textbook picture. Most long fibres on a free phage are folded back against the sheath, and probably only one to three of them bind receptors before the short fibres grab on. Only after contraction do the whiskers bend and release all six long fibres. (Hu, Margolin, Molineux & Liu (2015): Structural remodeling of bacteriophage T4 and host membranes during infection initiation, PNAS.)

T4 DNA contains no ordinary cytosine. Phage enzymes make 5-hydroxymethylcytosine (HMC) instead, and other phage enzymes then attach glucose to it. The sugar coat protects T4 DNA from many host restriction enzymes, and the difference lets T4 nucleases chop up the host's cytosine-containing DNA while leaving its own alone. (Miller et al. (2003): Bacteriophage T4 genome, Microbiology and Molecular Biology Reviews.)

The T4 genome is 168,903 base pairs and codes for about 300 gene products: 289 probable protein-coding genes, 8 tRNA genes and a few other small RNAs. Its genes are switched on in three waves, from 39 early, 30 middle and 50 late promoters. Middle genes need the phage activator MotA; late genes, which code for the head, tail and fibres, need a phage sigma factor, gp55. (Miller et al. (2003): Bacteriophage T4 genome, Microbiology and Molecular Biology Reviews.)

An empty T4 head is filled by a motor that docks on the portal vertex. The large terminase, gp17, forms a five-subunit ring that burns ATP to thread the DNA in at up to 2,000 base pairs per second, so the whole genome goes in in about 5 minutes. The motor can push against forces of about 60 piconewtons, which makes it, scaled up, about twice as powerful as a car engine. (Rao & Black (2010): Structure and assembly of bacteriophage T4 head, Virology Journal.)

Packing stops when the head is full, not when a particular DNA sequence is reached. That 'headful' rule means each head holds about 1.02 genome lengths. The extra bit is a repeat of the start of the genome at the end (terminal redundancy), and because each new head starts packing where the last one stopped, every phage's DNA starts at a different place (circular permutation). The DNA ends up at about 500 mg/ml, with neighbouring duplexes 2.5 nm apart, like a liquid crystal. (Rao & Black (2010): Structure and assembly of bacteriophage T4 head, Virology Journal.)