Question: How many ways can some bacteria be transfered between cells?
About the article "Bacteria", section "DNA transfer".

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Almost all bacteria are invisible to the naked eye, with a few extremely rare exceptions, such as "Thiomargarita namibiensis".
They lack a nucleus and other membrane-bound organelles, and can function and reproduce as individual cells, but often aggregate in multicellular colonies.
Their genome is usually a single loop of DNA, although they can also harbor small pieces of DNA called plasmids.
These plasmids can be transferred between cells through bacterial conjugation.
Bacteria are surrounded by a cell wall, which provides strength and rigidity to their cells.
They reproduce by binary fission or sometimes by budding, but do not undergo meiotic sexual reproduction.
However, many bacterial species can transfer DNA between individual cells by a process referred to as natural transformation.
(Also see Transformation (genetics)).
In nature, the development of competence for transformation is usually associated with stressful environmental conditions, and seems to be an adaptation for facilitating repair of DNA damage in recipient cells.
(Also see Natural competence.)
Some species form extraordinarily resilient spores, but for bacteria this is a mechanism for survival, not reproduction.
Under optimal conditions bacteria can grow extremely rapidly and can double as quickly as every 20 minutes. 
Publications describing use of IMC in microbiology began in the 1980s (Jesperson 1982).
While some IMC microbiology studies have been directed at viruses (Heng et al.
2005) and fungi (Antoci et al.
1997), most have been concerned with bacteria.
A recent paper (Braissant et al.
2010) provides a general introduction to IMC metabolismic methods in microbiology and an overview of applications in medical and environmental microbiology.
The paper also explains how heat flow vs. time data for bacteria in culture are an exact expression—as they occur over time—of the fluctuations in microorganism metabolic activity and replication rates in a given medium (Fig.
In general, bacteria are about 1/10 the size of mammalian cells and produce perhaps 1/10 as much metabolic heat-i.e.
ca.
3x10−12 W/cell.
Thus, compared to mammalian cells (see above) ca.
10X as many bacteria—ca.
330,000—must be present to produce detectable heat flow—i.e.
1 μW.
However, many bacteria replicate orders of magnitude more rapidly in culture than mammalian cells, often doubling their number in a matter of minutes (see Bacterial growth).
As a result, a small initial number of bacteria in culture and initially undetectable by IMC rapidly produce a detectable number.
For example, 100 bacteria doubling every 20 minutes will in less than 4 hours produce >330,000 bacteria and thus an IMC-detectable heat flow.
Consequently, IMC can be used for easy, rapid detection of bacteria in the medical field.
Examples include detection of bacteria in human blood platelet products (Trampuz et al.
2007) and urine (Bonkat "et al."
2011) and rapid detection of tuberculosis (Braissant et al.
2010, Rodriguez et al.
2011).
Fig.
7 shows an example of detection times of Tuberculosis bacteria as a function of the initial amount of bacteria present in a closed IMC ampoule containing a culture medium.
For microbes in growth media in closed ampoules, IMC heat flow data can also be used to closely estimate basic microbial growth parameters; i.e.
maximum growth rate and duration time of the lag phase before maximum growth rate is achieved.
This is an important special application of the basic analysis of these parameters explained previously (Overview (Data Obtained)).
"Unfortunately, the IMC literature contains some published papers in which the relation between heat flow data and microbial growth in closed ampoules has been misunderstood.
However, in 2013 an extensive clarification was published, describing (a) details of the relation between IMC heat flow data and microbial growth, (b) selection of mathematical models which describe microbial growth and (c) determination of microbial growth parameters from IMC data using these models (Braissant et al.
2013)."
The T3SS in many bacteria has been manipulated by researchers.
Observing the influence of individual manipulations can be used to draw insights into the role of each component of the system.
Examples of manipulations are:  Deletion of one or more T3SS genes (gene knockout).
Overexpression of one or more T3SS genes (in other words: production "in vivo" of a T3SS protein in quantities larger than usual).
Point or regional changes in T3SS genes or proteins.
This is done in order to define the function of specific amino acids or regions in a protein.
The introduction of a gene or a protein from one species of bacteria into another (cross-complementation assay).
This is done in order to check for differences and similarities between two T3SSs.
Manipulation of T3SS components can have influence on several aspects of bacterial function and pathogenicity.
Examples of possible influences:  The ability of the bacteria to invade host cells, in the case of intracellular pathogens.
This can be measured using an invasion assay (gentamicin protection assay).
The ability of intracellular bacteria to migrate between host cells.
The ability of the bacteria to kill host cells.
This can be measured by several methods, for instance by the LDH-release assay, in which the enzyme LDH, which leaks from dead cells, is identified by measuring its enzymatic activity.
The ability of a T3SS to secrete a specific protein or to secrete at all.
In order to assay this, secretion is induced in bacteria growing in liquid medium.
The bacteria and medium are then separated by centrifugation, and the medium fraction (the supernatant) is then assayed for the presence of secreted proteins.
In order to prevent a normally secreted protein from being secreted, a large molecule can be artificially attached to it.
If the then non-secreted protein stays "stuck" at the bottom of the needle complex, the secretion is effectively blocked.
The ability of the bacteria to assemble an intact needle complex.
NCs can be isolated from manipulated bacteria and examined microscopically.
Minor changes, however cannot always be detected by microscopy.
The ability of bacteria to infect live animals or plants.
Even if manipulated bacteria are shown "in vitro" to be able to infect host cells, their ability to sustain an infection in a live organism cannot be taken for granted.
The expression levels of other genes.
This can be assayed in several ways, notably northern blot and RT-PCR.
The expression levels of the entire genome can be assayed by microarray.
Many type III transcription factors and regulatory networks were discovered using these methods.
The growth and fitness of bacteria.  
HeLa cells are commonly used as eukaryotic cells in the gentamicin protection assay, but other cells can be used as well.
As for bacteria, only species susceptible to gentamicin can be assayed.
The assay is performed in polypropylene plates with round wells, which are commonly used in laboratories for culturing eukaryotic cells.
The cells are allowed to grow in the wells overnight, creating a flat layer.
Bacteria are separately grown overnight.
On the next day the eukaryotic cells are inoculated with the bacteria and are incubated together for an hour.
Centrifuging the plates for a few minutes may help bring cells and bacteria in contact and initiate infection.
After infection gentamicin is added to the plates, and they are incubated for an hour, allowing the antibiotic to kill all bacteria that were not able to penetrate the cells and remained outside.
The plates are then washed well to remove the dead bacteria.
Next the eukaryotic cells are lysed using a detergent, most commonly Triton X-100.
The bacteria that penetrated the cells and remained alive are now released, and they are plated on solid medium plates.
Counting the colonies formed on the plates on the next day, and knowing how many bacteria were used in the beginning of the assay, enables the researcher to calculate the percentage of bacteria that were able to invade the eukaryotic cells. 
Bacterial mycophagy was a term coined in 2005, to describe the ability of some bacteria to "grow at the expense of living fungal hyphae".
In a 2007 review in the "New Phytologist" this definition was adapted to only include bacteria which play an active role in gaining nutrition from fungi, excluding those that feed off passive secretions by fungi, or off dead or damaged hyphae.
The majority of our knowledge in this area relates to interactions between bacteria and fungi in the soil and in or around plants, little is known about interactions in marine and freshwater habitats, or those occurring on or inside animals.
It is not known what affects bacterial mycophagy has on the fungal communities in nature.
There are three mechanisms by which bacteria feed on fungi; they either kill fungal cells, cause them to secrete more material out of their cells or enter into the cells to feed internally and they are categorised according to these habits.
Those that kill fungal cells are called nectrotrophs, the molecular mechanisms of this feeding are thought to overlap considerably with bacteria that feed on fungi after they have died naturally.
Necrotrophs may kill the fungi through digesting their cell wall or by producing toxins which kill fungi, such as tolaasin produced by "Pseudomonas tolaasii".
Both of these mechanisms may be required since fungal cell walls are highly complex, so require many different enzymes to degarde them, and because experiments demonstrate that bacteria that produce toxins cannot always infect fungi.
It is likely that these two systems act synergistically, with the toxins killing or inhibiting the fungi and exoenzymes degrading the cell wall and digesting the fungus.
Examples of necrotrophs include "Staphylococcus aureus" which feed on "Cryptococcus neoformans", "Aeromonas caviae" which feed on "Rhizoctonia solani", "Sclerotium rolfsii" and "Fusarium oxysporum", and some myxobacteria which feed on "Cochliobolus miyabeanus" and "Rhizoctonia solani".
Bacteria which manipulate fungi to produce more secretions which they in turn feed off are called extracellular biotrophs; many bacteria feed on fungal secretions, but do not interact directly with the fungi and these are called saprotrophs, rather than biotrophs.
Extracellular biotrophs could alter fungal physiology in three ways; they alter their development, the permeability of their membranes (including the efflux of nutrients) and their metabolism.
The precise signalling molecules that are used to achieve these changes are unknown, but it has been suggested that auxins (better known for their role as a plant hormone) and quorum sensing molecules may be involved.
Bacteria have been identified that manipulate fungi in these ways, for example mycorhizzal helper bacteria (MHBs) and "Pseudomonas putida", but it remains to be demonstrated whether the changes they make are cause are directly beneficial to the bacteria.
In the case of MHBs, which increase infection of plant roots by mycorrhizal fungi, they may benefit, because the fungi gain nutrition from the plant and in turn the fungi will secrete more sugars.
The third group, that enter into living fungal cells are called endocellular biotrophs.
Some of these are transmitted vertically whereas others are able to actively invade and subvert fungal cells.
The molecular interactions involved in these interactions are mostly unknown.
Many endocellular biotrophs, for example some "Burkholderia" species, belong to the β-proteobacteria which also contains species which live inside the cells of mammals and amoeba.
Some of them, for example "Candidatus" Glomeribacter gigasporarum, which colonises the spores of "Gigaspora margarita", have reduced genome sizes indicating that they have become entirely dependent on the metabolic functions of the fungal cells in which they live.
When all the endocellular bacteria inside "G. margarita" were removed, the fungus grew differently and was less fit, suggesting that some bacteria may also provide services to the fungi they live in.