Does Escherichia coli Have A Nose?

Paul Yeatman 1993.  Years later I found the paper I was supposed to have  found by JF Parkinson and DF Blair.  The article below knows nothing of  this one .

Introduction

In order to decide whether or not Escherichia coli has a nose, one may compare the sense of smell in higher organisms with the mechanisms involved in chemotaxis. Also one could examine chemotaxis on its own. When this is done it may be decided if E.coli can “smell” chemicals and respond to them. Such a discussion needs to involve the detection of chemoeffectors and how such detection results in flagellar rotation and subsequent cell movement. This is necessary as if it is not understood how chemotaxis works, one cannot form any ideas about the presence of a nose. It is unlikely the E.coli has a nose in the true sense, but it possibly has the bacterial version of one. Similarities exist between the substances detected (broadly) by both systems. A phenomenon known as adaptation operates in both the nose and chemotaxis. The behaviour of an animal resulting from various smells can be likened to the swim or tumble response seen in E.coli.

A cell displaying a chemotactic response is more likely to be virulent or invasive. This is related to the bacteria’s motility as well as its ability to detect host cells or organisms. Such is true in both an environmental and clinical situation, though some minor differences are present.

Comparison Of Smell And Chemotaxis

The sense of smell is the result of the interaction between olfactory hairs and odor producing molecules, and processing of the signal by the brain (Amoore 1970). The detection takes place on the olfactory cilia or exposed tip of the olfactory rod. Humans can detect several odor types, namely camphorous, floral, musk, ethereal, peppermint, putrid and pungent (Rhoades etal 1992). Molecular binding results in an action potential which travels along a nerve pathway to the brain for processing. Each olfactory receptor is specific for one type of odor. The olfactory system plays s role in appetite and eating and mating behavior. Usually odor chemicals from unfavorable environments are detected at much lower concentrations than those from favorable environments. For example, sulfur compounds in odors are detected at minute concentrations, due to their stopping breathing at high levels.

In E.coli, transmembrane receptors or transducers detect the chemicals responsible for chemotaxis (attractants and repellents), dissolved in situ. These transducers then cause cytoplasmic protein components to become methylated or phosphorylated. These components then control the flagellar switch proteins while others control adaption (Ninfa etal 1991).

In humans the nose detects smell via direct contact between odorous molecules and the detection cells. Odor producing molecules are diffuse volatile chemicals in the air and need to be solublised before their detection may occur via the olfactory cilia (Amoore 1970). The chemicals which initiate the chemotactic response in E.coli are also diffuse in their environment and are solublised in the growth media. Their detection is also via direct contact with the chemotactic transducers, or via interaction with a binding protein connected to a transducer. The transducer activated depends on the chemoeffector detected (Bourret etal 1991). In this way the detection of odor molecules and the detection of chemoeffectors which mediate chemotaxis is similar.

Both the sense of smell and chemotaxis exhibit a response to unchanging chemical concentrations over time known as adaption. Where smell is concerned this means that the action potential developed by odor molecules binding to their receptor gradually fades until the smell is no longer detected. In a bacterium, adaption is due to altered methylation levels of cytoplasmic components which turn off the transducer signal which excites the flagellar switch. This occurs when the chemical concentration in the growth media is constant over a period of time. Such a process allows E.coli to respond to a further change in chemical concentration. This process also requires E.coli to have a short term memory. This is necessary to compare present data with the past to tell whether the cell is moving toward an attractant or not. Such adaption is mediated by the two cytoplasmic proteins which are regulatory pathway specific (Bourret etal 1991).

It has been shown that perfumes and colones may attract the opposite sex in most animals (Rhoades etal 1992). Such odors will also stimulate things such as eating and sexual behavior. A putrid smell will repel an organism with a nose, while a floral scent may attract it. This is related to the pleasantness of the smell on a conscious level. On an unconscious level pheromones are to attract the opposite sex. This may be compared to the chemoeffectors of chemotaxis. An attractant will induce a cell to move toward it by increasing the cell’s swimming time, while a repellent will increase the cell’s tumbling, resulting in it moving away. Unlike smell, E.coli has no choice whether or not to move toward an attractant or away from a repellent. Despite this one can see that smell in animals and chemoeffectors in bacteria have a similar effect on each organism’s behavior. Also, an E.coli can detect the presence of F- cells (Bourret etal 1991). This enables the bacteria to move toward such cells and conjugate or “mate” with them.

The comparison of smell and some aspects of chemotaxis suggests that both processes are similar. As such E.coli may have a bacterial nose. For a more detailed discussion the actual mechanisms dictating smell detection and the chemotactic response would be required.

Discussion Of Chemotaxis

Detection Of Chemoeffectors

The chemicals which are responsible for the chemotactic response which are detected in the growth media are known as chemoeffectors. Such effectors are detected by proteins called transducers (Tsr, Tar, Trg and Tap) in the periplasmic space (Bourret etal 1991). Each transducer detects only a few types of chemoeffector. The chemoeffectors are classed as attractants and repellents. Serine, aspartate, maltose, ribose galactose and some dipeptides are attractants. Repellents are leucine, Co²⁺ and Ni²⁺. Tsr detects serine and leucine, Tar: aspartate, maltose, Co and Ni, Trg: ribose and galactose and Tap detects dipeptides. An attractant is treated as the opposite of a repellent. When a chemoeffector comes in contact with a transducer it will either bind directly to the transducer or bind via a binding protein. Such an interaction results in the transducer sending a signal to cytoplasmic components involved with chemotaxis (Bourret etal 1991).

Attractants are usually nutrients, while repellents are toxins or indicative of a toxic or unfavorable environment.

Cytoplasmic Component Functioning

The cytoplasmic components can be divided into two types. The first one is involved in the excitation pathway, while the second is involved in the adaption pathway. Two proteins, CheA and CheW are involved in both pathways and relay excitation signals to either CheY and CheZ involved in excitation, or CheR and CheB in adaption. CheA is sent signals from the transducers and CheW. It then sends signals to CheY and CheB (Bourret etal 1993). CheA is an autophosphorylating kinase which phosphorylates CheY. It is activated by CheW which is a coupling factor activated by the transducers (Dailey etal 1993). In order to phosphorylate CheA, CheW needs to act in conjuction with a divalent ion such as Mg²⁺ (Lukat etal 1990).

Excitation Pathway

CheA and CheW act to phosphorylate CheY. As CheA is phosphorylated, it needs to transfer its phosphate to CheY. To do this a divalent metal ion, (Cd²⁺, Mn²⁺, Zn²⁺, Co²⁺, Ca²⁺) is required to bind to CheY at a site just next to the phosphate binding site (Lukat etal 1990). This must mean that the ions somehow “grab” the phosphate on CheA and place it on CheY whilst holding onto CheY at the ion binding site. CheY-phosphate then increases the tumbling frequency of E.coli (Bourret etal 1991), while CheZ dephosphorylates CheY-phosphate with the aid of the metal ions once again and acts to increase the swimming frequency of the cell, (Dailey etal 1993). This means that CheY is a regulator, while CheZ is a suppresser. Both of these proteins act together to control flagellar switching and directly interact with the flagellar switching proteins, (Bourret etal 1991). Tumbling results from the flagella rotating in a clockwise direction, while counter clockwise rotation results in smooth swimming.

Adaption Pathway

Changes in the methylation levels of CheR and CheB are responsible for E.coli‘s ability to adapt to changes in chemoeffector concentration (Bourret etal 1991). Decreasing attractant concentration, (negative stimuli) decreases the methylation while increasing attractant concentration (positive stimuli) increases the methylation level. The altered methylation level stops the excitation signal, which allows the cell to adapt to new conditions (Bourret etal 1991). CheR is a methyltransferase while CheB is a methylesterase (Bourret etal 1991). These two proteins act in tandem to control adaption. Nonmethylated CheB blocks the transducer excitation signal, while CheR controls the methylation of CheB.

Flagellar Switching Proteins

The flagellar switching mechanism is composed of three proteins, FliG, FliM, FliN. These proteins are activated by CheY-phosphate and move to induce flagellar rotation in either the clockwise or counter clockwise direction (Bourret etal 1991).

Physiological Response Of Chemotaxis

The transducers, cytoplasmic components and switching proteins all work together to produce a physiological response in E.coli manifested as cell movement. If a cell detects an attractant such as ribose (a sugar and thus nutrient), CheY-phosphate will be blocked by CheZ. This acts to produce longer periods of swimming in the cell. Due to this, E.coli will tend to move toward the nutrient along an increasing chemical gradient, in this case ribose. If the concentration of ribose decreased or the concentration of a repellent, say leucine increased, CheZ would not be able to adequately block CheY-phosphate. This is due to CheY-phosphate being produced at a greater rate than CheZ removes the phosphate. This is related to the changes in methylation of CheW and CheA resulting from the extent of positive or negative stimuli. The tumbling action (produced by CheY-phosphate), acts to change the cell’s direction. By sampling solute concentrations, and then resampling at a different location, E.coli can build up a three dimensional picture of its chemical (concentration) environment. Once this has been done, the cell can decide where a more suitable environment is, and migrate there by decreasing the amount of phosphorylated CheY, thus enabling CheZ to induce swimming behavior.

It is interesting to note that Co²⁺ is a repellent (Bourret etal 1991), but also can facilitate the binding and removal of phosphate from CheA and CheY (Lukat etal 1990). Perhaps in too great a concentration, Co²⁺ disrupts the swim tumble process to such an extent that the E.coli either swim constantly, or tumble constantly, or have no defined ratio of tumbling to swimming. In either case, the result is not favorable to the cell’s survival. Constant tumbling would result in the cell doing “doughnuts” regardless of the concentration of attractants or repellents. Non stop swimming is slightly better as the cell may eventually encounter low levels of Co²⁺ and thus return to its normal chemotactic state. Erratic behavior may result in the cell entering a toxic environment and dying before low levels of Co²⁺ were encountered and normal functioning could occur. This is all based on the supposition that Co²⁺ is a repellent due to it disrupting E.coli‘s normal chemotactic response in too high a concentration. On the other hand, Co²⁺ may just be a repellent as it indicates the presence of toxins which could harm the cell.

 

Environmental And Clinical Infection

By looking at the chemotactic response, one sees that bacteria are attracted by an increasing chemical gradient of chemoeffectors called attractants. In an infection process, the presence of chemotaxis is an important factor. This can be observed with Pseudomonas syringae subspecies savastanoi, which causes olive and oleander galls, (Soby etal 991).

P.syringae subsp savastanoi, can detect chemical concentrations in its environment and use them via chemotaxis. If the roots of an olive or oleander are damaged somehow, they will secrete amongst their juices, chemoeffectors. The bacteria will detect these and move toward the damaged roots as they offer a more favorable growth environment. Here the presence of the chemotactic response allows a bacteria to initiate an infection, which otherwise may not have occurred if the bacteria was non motile.

In a clinical infection, the detection of chemoeffectors is much the same. However, an infection may occur from a contaminated object creating a wound and depositing the infectious agent, or the wound may be infected later by a chemoeffector sensing bacterium. In the case of a bacteria possessing chemotaxis, it will detect wound excretions and migrate to the site. As the host offers a better environment in which to grow, the bacterium will grow and produce an infection. Once again, if motility was not present, it is unlikely that an infection would be initiated.

Conclusions

The comparison of the sense of smell and some chemotactic aspects would suggest that E.coli has some sort of smell mechanism. Such a mechanism would only bear a passing resemblance to a nose. To determine if this is so, an in-depth examination of the sense of smell and chemotaxis would be required.

E.coli may have a nose if one substituted “smell” for “chemoeffector”. The “smell” of nutrients would then attract E.coli, while the smell of toxins or unfavorable environments would cause the cell to find a better location. The actual detection mechanisms of chemoeffectors and odor producing molecules are vastly different. However, depending on one’s definition of nose, E.coli quite possibly has a bacterial nose. Such an apparatus may have been the ancestor of what is known as a nose in higher organisms.

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