7.3: Specific Defenses - Biology

7.3: Specific Defenses

Under the Radar Screen: How Bugs Trick Our Immune Defenses

To ensure their own survival, viruses, bacteria, and parasites have devised ways to evade the immune surveillance of their respective host. By looking at the specific ways by which these microbes defeat the immune system and the molecular mechanisms that are under attack, the course aims to explore both host-pathogen interaction as well as gain insight into how the immune system operates when faced with such a challenge. (Image courtesy of Dr. G. Grotenbreg.)


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7.3: Specific Defenses - Biology

The pH of the female reproductive tract is also slightly acidic. How do sperm survive there?

Histamine release and temperature response. Are runny noses and fever , in themselves, a bad thing?

Phagocytes ( leukocytes including neutrophils, monocytes, and eosinophils) destroy foriegn cells in various ways including engulfing and by secreting lysosomal enzymes.

Leukocytes in general must be able to distinguish cells of the body (self) from cells of disease-causing organisms. Why?

Immune cells repond to any cells WITHOUT the set of surface proteins (major histocompatibility markers) on the cell membrane unique to all cells of the body in each individual.

i.e. These proteins mark cells of the body as SELF, analogous to a military uniform used to identify one's own countryman.

There are over 100 different forms (alleles) of MHC in the human population.

Why is it likely that a transplanted tissue is will be rejected unless the donor and recipient are closely related?

What would be a more effective weapon: one that is designed to combat anything that is recognized as foreign, or one that is designed to combat a specific invading threat?

Third Line of Defense - Acquired Immunity : Specific responses to specific threats

  • A specific antigen (the macromolecule, typically part of the DCO, that elicits an immune response) can only activate specific B and T cells . Of millions of B and T cells types produced by the body, one type that is specific for destroying a particular type of disease causing organism is rapidly produced in the presence of that specific antigen of the DCO. The race is on.
  • The antigen must be exposed to a helper T cell before the specific type of B cell or cytotoxic T cell (both of which must also be exposed to the antigen) can begin to multiple rapidly (i.e. is stimulated). This provides a 'check' prior to initiating a major immune response. What cell type is critical in this response and what disease disables this cell type?
  • There are two general responses: antibody-mediated B cell response and cell-mediated T cell response (see descriptions at bottom of the above diagram).
  • Memory cells are produced that are specific to that antigen and result in a much faster response to the disease in the event of future infections (i.e. immunity to that disease is conferred). Why faster?

if poor, then -slow response to disease-causing organisms

- cancer (the bodies own cells dividing out of control)

- allergies (immune response to non-dangerous substance) Why are allergies more common in developed nations?

- autoimmune diseases (the immune system attacks cells of the body)

- reproductive failures (sperm and fetal tissue can be recognized by the immune system as non-self Why? How is rejection prevented? )

Defense Mechanism in Plants (With Diagram) | Botany

In plants some structures are already present to defend the attack while in others, the structures to defend the host develops after the infection. In this way, structural defense can be characterised as (A) Preexisting defense structures and (B) Defense structures developed after the attack of the pathogen.

(A) Preexisting Defense Structures:

Wax-mixtures of long chain aliphatic compounds get deposited on the cuticular surface of some plants. Deposition of wax on the cuticular surface is thought to play a defensive role by forming a hydrophobic surface where water is repelled.

As a result, the pathogen does not get sufficient water to germinate or multiply. In addition, a negative charge usually develops on the leaf surface due to the presence of fatty acids – the main component of cuticle. The negative charge prevents/reduces the chance of infection by many pathogens.

The thickness of cuticle is most important for those which try to enter the host through the leaf surface. The cuticle thickness obstructs the path of pathogen. In addition, a thick cuticle checks the exit of the pathogen from inside the host, thus reducing the secondary infection.

(iii) Structure of Epidermal Cell Walls:

Tough and thick outer walls of epidermal cells may directly prevent the entry of the pathogen completely or make the entry difficult. The presence or absence of lignin and silicic acid in the cell walls may show variation in resistance to penetration of the pathogen.

Most outer walls of epidermal cells of rice plants are lignified and are seldom penetrated by blast disease of rice pathogen. In resistant varieties of potato tubers (resistant to Pythium debaryanum) the epidermal cells contain higher fibre content than the susceptible ones.

(iv) Structure of Natural openings:

Structure of natural openings like stomata lenticels etc. also decide the fate of the entry of the pathogen. In Szincum variety of citrus, the stomata are small and possess very narrow openings surrounded by broad lipped raised structures which prevent entry of water drops containing citrus canker bacterium.

In the same way, the size and internal structures of lenticels may play a defensive role against the pathogens. Varieties having small lenticels in the apple fruits prevent the entry of the pathogen while those having large openings easily allow the pathogen to enter.

Nectaries provide openings in the epidermis and may play a defensive role due to high osmotic concentration of the nectar. In resistant varieties of apple, presence of abundant hairs in the nectaries acts as a defense mechanism while susceptible varieties are devoid of abundant hairs.

Internal Defense Structures:

There are many preexisting internal defense structures inside the plant that prevent the entry of pathogen beyond these structures. In some plants, cell walls of certain tissues become thick and tough due to environmental conditions and this makes the advance of the pathogen quite difficult.

In case of stems of cereal crops, vascular bundles or extended areas of sclerenchyma cells checks the progress of rust pathogen. Leaf veins effectively obstruct the spread of pathogen like the angular leaf spot pathogen.

(B) Defense Structures Developed after the Attack of the Pathogen:

After the pathogen has successfully managed to overcome the preexisting defense mechanisms of the host, it invades the cells and tissues of the host.

In order to check the further invasion by the pathogen, the host plants develop some structures/mechanisms which may be defense reactions in the cytoplasm, cell wall defense structures, defense structures developed by the tissues and ultimately the death of the invaded cell i.e. necrosis. These will be briefly discussed here.

(i) Defense Reactions in the Cytoplasm:

The cytoplasm of the invaded cell surrounds the hyphae of the pathogen and the nucleus of the host cell gets stretched to break into two. In some host cells, the cytoplasm and the nucleus of the infected cells enlarge.

The cytoplasm becomes granular and dense and develops granular particles. These result in the disintegration of the pathogen mycelium and thus the invasion stops. Such cytoplasmic defence mechanisms can be seen in weak pathogens like Annillaria and some mycorrhizal fungi.

(ii) Cell Wall Defense Structures:

Cell wall defense structures are of limited help to the host. These include morphological changes in the cell wall of the host.

Three types of cell wall defense structures are generally observed:

(i) Cell walls thicken in response to the pathogen by producing a cellulose material, thus preventing the entry of the pathogen

(ii) The outer layer of cell walls of the parenchyma cells in contact with invading bacterial cells produce an amorphous fibrillar material that traps the bacteria thus preventing them to multiply and

(iii) Callose papillae get deposited on the inner layers of the cell walls due to invasion by fungal pathogens.

In raw cases, the hyphal tips of the infecting fungal pathogen penetrating the cell wall and thereafter growing into the cell lumen get enveloped by callose material that, later become infused with phenolics forming a sheath around the hyphae.

(iii) Defense Structures Developed by the Tissues:

The following four developments take place in the tissues after penetration:

(a) Gum Deposition:

Plants produce a variety of gummy substances around lesions or spots as a result of infection. These gummy substances inhibit the progress of the pathogen. The gummy substances are commonly produced in stone fruits.

(b) Abcission Layers:

Abscission layers are usually formed to separate the ripe fruits and old leaves from the plant. But in some stone fruit trees, these layers develop in their young leaves in response to infection by several fungi, bacteria or viruses. An abscission layer is a gap formed between two circular layers of cells surrounding the point of infection.

This gap is created by the dissolution of one or two layers of the middle lamella, one or two layers of cells surrounding the infected loci resulting in the infected locus becoming unsupported, shrivels, dies and falls down along with the pathogen. Abscission layer formation protects the healthy leaf tissue from the attack of the pathogen.

Tyloses are out growths of protoplasts of adjacent live parenchyma cells protruding into xylem vessels through pits under stress or in response to attack by the vascular pathogens. Their development blocks the Xylem vessels, obstructing the flow of water and resulting in the development of wilt symptoms.

However, tyloses are formed in some resistant plants ahead of infection and the prevent the plant from being attacked.

(D) Formation of Layers:

Some pathogens like certain bacteria, some fungi and even some viruses and nematodes stimulate the host to form multilayered cork cells in response to infection, these develop as a result of stimulation of host cells by substances secreted by thus, pathogen.

These layers inhibit the further invasion by the pathogen and also block the flow of toxic substances secreted by the pathogen. Cork layers also stop the flow of nutrients of the host thus also depriving the pathogen of the nutrients.

Examples of cork layer formation as a result of infection are: soft not of potato caused by Rhizopus sp., potato tuber disease caused by Rhizoctonia sp., Scab of potato caused by Streptomyces scabies and necrotic lesions on tobacco caused by tobacco mosaic virus.

IV. Necrosis or Hypersensitive Type of Defense:

Necrosis or hypersensitive type of defense is another defense mechanism adopted by some pathogens like Synchytrium endobioticum causing wart disease of potato, Phytophthora infestans causing late blight disease of potato and Pyricularia oryzae causing blast of rice etc.

In such diseases, the host nucleus moves toward the pathogen when the latter comes in contact with the protoplasm of the host. The nucleus soon disintegrates into brown granules which first accumulate around the pathogen, later dispersing throughout the host cytoplasm.

Soon the cell membrane swells and finally the cell bursts and dies. These cause the pathogen nucleus to disintegrate into a homogenous mass and its cytoplasm dense. As a result, the pathogen fails to grow beyond the necrotic or dead cells and the further growth of the pathogen is stopped.

II. Biochemical Defense:

Although structural defense mechanisms do prevent the attack of the pathogen, the defense mechanism also includes the chemical substances produced in the plant cells before or after the infection.

It has now been established that biochemical defense mechanisms play more important role than the structural defense mechanisms. This has been supplemented by the fact that many pathogens entering non host plants naturally or artificially inoculated fail to cause infections in absence of any structural barriers.

This does suggest that chemical defense mechanisms rather than structural mechanisms are responsible for resistance in plants against certain pathogens.

(A) Preexisting Biochemical Defense:

(i) Inhibitors Released in the Prepenetration Stage:

Plant generally exudes organic substance through above ground parts (phyllosphere) and roots (rhizosphere). Some of the compounds released by some plants are known to have an inhibitory effect on certain pathogens during the prepenetration stage.

For example fungistatic chemicals released by tomato and sugar beet prevent the germination of Botrytis and Cercospora. Presence of phenolics like protocatechuic acid and catechol in scales of red onion variety inhibit the germination of conidia of Colletotrichum circinans on the surface of red onion.

Inhibitors present in high concentrations in the plant cells also play an important role in defense of plants. Presence of several phenolics, tannins and some fatty acid like compounds such as dienes in cells of young fruits, leaves or seeds afford them resistance to Botrytis.

The tubers of resistance vars of potato against potato scab disease contain higher concentrations of chlorogenic acid around the lenticels and tubers than the susceptible vars. Several other compounds like saponin tomatin in tomato and avinacin in oats have antifungal activity. Some enzymes like glucanases and chitinases present in cells of some plants may break down the cell wall components of pathogens.

(ii) Lack of nutrients essential for the pathogen is another preexisting biochemical defense mechanism. Plant varieties or species which do not produce any of the chemicals essential for the growth of pathogen may act as resistant variety.

For example, a substance present in seedling varieties susceptible to Rhizoctonia initiates hyphae cushion formation from which the fungus sends penetration hyphae inside the host plants. When this substance is not present, hyphal cushions are not formed and the infection does not occur.

(iii) Absence of Common Antigen in Host plant:

It is now clear that the presence of a common protein (antigen) in both the pathogen and host determines diseases occurrence in the host. But if the antigen is present in the host and absent in the host or vice-versa, it makes the host resistant to the pathogen.

For example, varieties of linseed which have an antigen common to their pathogen are susceptible to the disease rust of linseed caused by Melampsora lini.

In contrast, the absence of antigen in linseed varieties but occurring in the pathogen are resistant to the pathogen. Another example is leaf spot disease of cotton caused by Xanthomonas campestris pv. malvacearum.

(B) Post-Infection-Biochemical Defense Mechanism:

In order to sight infections caused by pathogens or injuries caused by any other means, the plant cells and tissues produce by synthesis many substances (chemicals) which inhibit the growth of causal organism.

These substances are generally produced around the site of infection or injury with the main aim at overcoming the problem.

Some such important chemicals are described below:

These are the most common compounds produced by plants in response to injury or infection. The synthesis of phenolic compounds takes place either through “acetic acid pathway” or “Shikimic acid pathway”.

Some common phenolic compounds toxic to pathogens are chlorgenic acid, caffeic acid and ferulic acid. These phenolic compounds are produced at a much faster rate in resistant varieties than in susceptible varieties.

Probably that the combined effect of all phenolics present is responsible for inhibiting the growth of the infection.

Phytoalexins are toxic antimicrobial substances synthesized ‘de novo’ in the plants in response to injury, infectious agents or their products and physiological stimuli. The term phytoalexin was first used by the two phytopathologists Muller and Borger (1940) for fungi static compounds produced by plants in response to mechanical or chemical injury or infection.

All phytoalexins are lipophilic compounds and were first detected after a study of late blight of potato caused by Phytophthora infestans. Phytoalexins are believed to be synthesized in living cells but surprisingly necrosis follows very quickly.

According to Bill (1981), peak concentration of phytoalexins almost always coincides with necrosis. Although the exact mechanism of production of phytoalexin has not been properly understood, it is considered that a metabolite of the host plant interacts with specific receptor on the pathogen’s membrane resulting in the secretion of “phytoalexin elicitor” which enters the host plant cells and stimulates the phytoalexin synthesis.

Phytoalexins are considered to stop the growth of pathogens by altering the plasma membrane and inhibiting the oxidative phosphorylation.

Phytoalexins have been identified in a wide variety of species of plants such as Soyabean, Potato, sweet potato, barley, carrot, cotton etc. are being investigated. Some common phytoalexins are Ipomeamarone, Orchinol, Pistatin, Phaseolin, Medicarpin, Rishitin, Isocoumarin, ‘Gossypol’ Cicerin, Glyceolin, Capisidiol etc.

The following Table gives a list of phytoalexins, chemical nature the host and the pathogens in response to which these are produced:

(iii) Substances Produced in Host to Resist Enzymes Produced by Pathogen:

Some hosts produce chemicals which neutralise the enzymes produced by pathogen, thus defending the host. Therefore these substances help plants to defend themselves from the attack of the pathogen.

In bean plants, infection with Rhizoctonia solani causes necrosis. In resistant bean varieties, the entry of pathogen causes the separation of methyl group from methylated pectic substances and forms polyvalent cations of pectic salts which contain calcium.

The calcium ions accumulate in infected as well as neighbouring healthy tissues and because of the calcium accumulation, the pathogen fails to disintegrate middle lamella by its polygalacturonase enzymes. These are known to dissolve the middle lamella of healthy tissue in susceptible varieties.

(iv) Detoxification of Pathogen Toxins and Enzymes:

In some cases, the plants produce chemicals which deactivate the toxins produced by the pathogens. For example, Pyricularia oryzae which causes blast disease of rice produces Picolinic acid and pyricularin as toxins.

Although resistant varieties convert these toxins into N-methyl picolininic acid pyrecularin into other compounds, the susceptible varieties do get affected by these toxins. Similarly in case of cotton and tomato wilts, the toxin fusaric acid produced by the pathogen gets converted into non-toxic N-methyl-fusaric acid amide in resistant varieties.

As in case of detoxification of toxins, the toxic enzymes produced by the pathogen is deactivated by phenolic compounds or their oxidation products. Some varieties of cider apple are resistant to brown not disease caused by Sclereotiniafructigena.

It may be because of the resistant varieties producing pheolic oxidation products which inactivate the pectinolytic enzymes produced by the pathogen.

(v) Biochemical Alterations:

It has been observed that infection of the host by the pathogen brings about biochemical changes in the host which may prove toxic to the pathogenic microorganisms and cause resistance to the pathogen. Production of certain new enzymes and other compounds are synthesized and accumulated in higher concentration. This may also add to the resistance of the plant by being toxic to pathogenic microorganisms.


In vertebrates, in addition to the highly specialized and specific mechanisms of the adaptive immune system, a first line of defense constituted by the innate immune system involves the recognition of different classes of pathogens via germline-encoded proteins such as the Toll-like receptors [35]. The degree to which invertebrates are also able to respond specifically to infection is a question of considerable interest [36]. In this study we investigated whether infection of C. elegans by taxonomically distinct bacterial pathogens provokes distinct changes in gene expression. A principal motivation for the study was the difficulty in drawing conclusions from comparisons between studies using different experimental designs. For example, of a total of 392 genes reported to be induced in worms infected with P. aeruginosa in two independent studies, less than 20% were found in both [10, 11]. With regards to our own results, there was essentially no overlap between the genes or gene classes found to be up-regulated by S. marcescens in this and a previous study [8].

Through the use of exploratory analyses, we identified genes that are regulated differentially by the pathogens used in this study. Employing three biologically replicated datasets from synchronized populations at a single time-point and the computational methods described, a robust statistical significance could not be ascribed to changes in individual gene expression associated with the pathogen-specific responses. This is probably because the datasets for individual pathogens were relatively small and contained inherent experimental variation. Nevertheless, a strong trend emerged from the groups of non-overlapping genes that define these responses, and when combined with results from previous studies [8–11] strongly suggest that C. elegans is capable of mounting a distinct response to different bacterial pathogens.

In contrast to the above, with the use of these same statistical tools we were able to define a group of common response genes having similar expression profiles across infections with three different pathogens (Table 1). We consider this high-confidence group to be a minimum set, since it is possible that a more extensive study employing more replication in the experimental design, different time-points or changed for other parameters would reveal additional genes to be commonly regulated by multiple pathogens. Pathogens that vary considerably in their virulence and that provoke different symptoms were used. Therefore, in the context of this study, common response genes are potentially constituents of mechanisms underlying a pathogen-shared, host-response to different infections. Many of these genes have been functionally characterized as participating in the response of C. elegans to various forms of stress as well as to infection by bacterial pathogens. Specific examples include lys-1 and clec-63, a lysozyme and C-type lectin, respectively. Both the lysozyme and C-type lectin classes of genes are known to have roles in innate immunity [8, 9]. The expression of lys-1 is also modulated by insulin signaling [37] and by a toxin-induced stress response [38]. Taken as a whole, this suggests that common response genes may be regulated not only as a direct result of infection, but also by other factors consequent upon infection.

On the other hand, common response genes are not induced by infection with the fungus D. coniospora. Indeed, the signature of gene transcription associated with fungal infection is completely different from that provoked by the four bacterial pathogens used in this study. As discussed above, the antimicrobial peptide gene, nlp-29 is induced only by D. coniospora. We had previously reported that a second antimicrobial peptide gene, cnc-2, was induced upon infection both by S. marcescens and D. coniospora, based on our results using cDNA microarrays [27]. cnc-2 was found to be up-regulated by P. aeruginosa infection [10] and suggested to be a 'general response gene'. Like nlp-29, cnc-2 appeared not to be up-regulated by any of the bacterial pathogens used in this study, nor in our hands by P. aeruginosa (CL Kurz, personal communication). Nor was cnc-2 induced by high osmolarity (OZugasti, personal communication). On the other hand, the structurally related gene cnc-7 is up-regulated under conditions of osmotic stress (T Lamitina, personal communication). The cDNA microarrays we used previously do not have a cnc-7-specific probe, but the sequence of the cnc-7 mRNA is >80% identical to that of cnc-2. Therefore, it is possible that dry plate conditions induced cnc-7 expression and cross-hybridization resulted in the erroneous detection of increased cnc-2 transcript levels.

As mentioned previously, the down-regulated common response genes identified in this study appear to have functions associated with general metabolism. For example, the genes that show the greatest down-regulation, acdh-1 and -2, encode acyl-CoA dehydrogenases involved in mitochondrial β-oxidation and the metabolism of glucose and fat. Their expression levels are also repressed upon starvation [39, 40]. The modulation of their expression by pathogens could reflect a reduction in food uptake upon infection, or be part of a mechanism to control cellular resources and limit their availability to pathogens. The role that transcriptional repression plays in the innate immune response of C. elegans must be the subject of future studies.

Common response genes identified in this study include a grouping of seven genes associated with proteolysis and cell death, asp-1, 3, 4, 5 and 6, T28H10.3 and Y39B6A.24. With the exception of Y39B6A.24, all others are known to be expressed in the intestine (supplementary Table 3b in Additional data file 3). Using information from the Pfam database [41], all seven have been annotated as possessing a potential amino-terminal signal sequence. Interestingly, the remaining member of the aspartyl protease-encoding ASP family, ASP-2, which is not part of the pathogen-shared response, does not possess a comparable signal-sequence. While some aspartyl proteases within the cathepsin Esub-family are known to be secreted into the nematode intestine [42], experimental observations with full-length GFP fusions for ASP-3 and -4 indicate a predominantly lysosomal localization [17]. This suggests that the intracellular targeting of up-regulated proteases to lysosomes and perhaps other sub-cellular organelles, such as mitochondria, may be crucial for their proper functioning.

In C. elegans, necrosis is the best characterized type of non-apoptotic cell death [18]. Necrotic cell death is triggered by a variety of both extrinsic and intrinsic insults and is accompanied by characteristic morphological features. Our findings provide the first description of pathogen-induced necrosis in this model organism. While necrosis has been associated with infection in other metazoans, its role during infection remains unclear. Necrosis has been implicated in defensive or reparative roles following cellular damage, and necrotic cell death in tissues that have been compromised after vascular-occlusive injury triggers wound repair responses [43]. Successful pathogens overcome physical, cellular, and molecular barriers to colonize and acquire nutrients from their hosts [44]. In such interactions, it has been suggested that the cellular machinery of the host may in fact be exploited by viral and bacterial pathogens that induce necrotic cell death, resulting in damage to host tissue. For example, during Shigella-mediated infection, necrosis-associated inflammation is induced within intestinal epithelial cells of the host by the pathogen [45].

Our results suggest that in C. elegans, some experimental bacterial infections provoke a common program of gene regulation with consequences that include the promotion of necrosis in the intestine. Thus, these bacteria appear to exploit the necrotic machinery of C. elegans via a common host mechanism. While pathogen-induced necrosis might be protective for some infections, for the two bacteria tested, it appears to have no protective role and apparently hastens the demise of the host during the course of infection. Although there is increasing evidence for co-evolution between C. elegans and S. marcescens [7, 46], and E. carotovora, E. faecalis and P. luminescens can be found in the soil [47–49], there is no reason to believe that the bacteria used in this study developed virulence mechanisms to induce necrosis specifically in C. elegans.

In many cases, groups of genes that function together in the host response to pathogens or parasites share common regulation [11, 50]. We sought to identify other genes that potentially function alongside common response genes within the intestine, but that were not identified for whatever reason as being transcriptionally regulated in this study. These include those having the potential for common transcriptional regulation. Unfortunately, there is still no simple relationship between transcriptional co-regulation and regulatory motifs [51]. Efforts are being made to this end, however, and data for regulatory motifs in C. elegans are available within the cis-Regulatory Element Database (cisRED) [52]. Relevant information could be obtained for only five common response genes expressed in the intestine (supplementary Table 4a in Additional data file 3). These are associated via shared, predicted motif groups with a number of other intestinally expressed genes (Figure 6 supplementary Table 4b in Additional data file 3). All five common response genes are associated with biological themes relevant to infection (see Results) and we observed similar associations with a number of the genes having shared genomic motifs (Figure 6 supplementary Table 4c in Additional data file 3). We postulate that these genes, associated with common response genes on the dual basis of shared motifs, found within genomic regions conserved across closely related species, and functional relevance, may potentially be intestine-localized components of a pathogen-shared response.

Modeling the molecular basis underlying an intestine-localized, pathogen-shared response to infection in C. elegans. Three major components make up the model the common response genes identified directly in this study, genes associated with common response genes on the basis of shared DNA motifs, and interactors of the common response genes, either genetic (Wormbase) or physical (core or scaffold InteractomeDB). Unambiguous evidence for expression in the intestine exists for all indicated genes. The relevant biological functions are shown in different colors.

We also took advantage of published interaction data from InteractomeDB [53, 54] and WormBase [55], to identify other genes and proteins that could potentially function alongside common response genes within the intestine. Of all common response genes expressed in the intestine, relevant interaction networks could be established only for asp-3 and asp-6 (Figure 6 supplementary Table 4d in Additional data file 3). With the exception of the interaction between ERM-1 and ASP-3 that was identified in a large-scale study, all other interactions shown have additional evidence obtained via small-scale studies. ERM-1 appears to be primarily involved in the maintenance of intestinal cell integrity abrogation of erm-1 function by RNAi provokes distortion of the intestinal lumen in the adult animal [56]. In the case of itr-1 and crt-1, both have been implicated in the control of necrotic cell death [57] via regulation of intracellular calcium [18]. It follows that in the context of an interaction-network, their association with the common response gene asp-6 may be an indication of their involvement in intestinal cell necrosis provoked by infection. Such a possibility awaits experimental verification.


Body temperature increases as a protective response to infection and injury. An elevated body temperature (fever) enhances the body’s defense mechanisms, although it can cause discomfort.

A part of the brain called the hypothalamus controls body temperature. Fever results from an actual resetting of the hypothalamus's thermostat. The body raises its temperature to a higher level by moving (shunting) blood from the skin surface to the interior of the body, thus reducing heat loss. Shivering (chills) may occur to increase heat production through muscle contraction. The body's efforts to conserve and produce heat continue until blood reaches the hypothalamus at the new, higher temperature. The new, higher temperature is then maintained. Later, when the thermostat is reset to its normal level, the body eliminates excess heat through sweating and shunting of blood to the skin.

Certain people (such as alcoholics, the very old, and the very young) are less able to generate a fever. These people may experience a drop in temperature in response to severe infection.

After the establishment of infection in plant cells, the host defense tries to create barriers for further colonization of tissues.

This may be at various levels

1. Lignification:

  • The lignified cell wall provides an effective barrier to hyphal penetration.
  • The lignin layer in the cell wall thickens when pathogen gets an entry into the tissues.
  • Act as an impermeable barrier for free movement of nutrients causing starvation of the pathogen.

2. Suberization:

  • In several plants, the infected cells are surrounded by suberized cells. Thus isolating them from healthy cells.
  • Corky layer formation is a part of the natural healing system of plants.
  • Example: – Scab of potato and rot of sweet potato are good examples.

3. Abscission layers:

  • It is a gap between the host cell layers and devices for dropping-off old leaves and mature fruits.
  • The plant may use this for defense mechanism also i.e. to drop-off infected or invaded plant tissue or part.
  • Example: – a shot hole in the leaves of fruit trees is a common example.

4. Gum deposition:

  • The gums and vascular gels quickly accumulate and fill the intercellular spaces or within the cell surroundings the infection thread.

5. Tyloses:

  • They are formed by the protrusion of the xylem parenchymatous cells through pits into xylem vessels.
  • The tyloses are inductively formed much ahead of infection thus blocking the spread of the pathogen.

7.3: Specific Defenses - Biology

Application: tRNA-activating enzymes illustrate enzyme–substrate specificity and the role of phosphorylation.

  • these features allow tRNA to attach to binding sites on ribosomes and to mRNA
  • variable features in each type of tRNA produce different physical and chemical properties, allowing for the correct binding of amino acids to specific tRNAs
  • tRNA activating enzyme attaches a specific amino acid to the 3’ end of a tRNA
  • there are 20 different tRNA activating enzymes, one for each of the 20 amino acids
  • each of these enzymes attaches one particular amino acid to all of the tRNA molecules that have an anticodon corresponding to that amino acid
  • ATP hydrolysis provides the energy for amino acid attachment to tRNA this stored energy is also used later to link the amino acid to the growing polypeptide chain during translation

2. Synthesis of the polypeptide involves a repeated cycle of events.

  • tRNA with anticodon complementary to second mRNA codon binds to ribosomal A site, with appropriate amino acid attached to tRNA 3’ terminal
  • enzymes in ribosome catalyze formation of peptide bond between methionine and 2nd amino acid
  • P site tRNA, now separated from methionine, exits ribosome
  • ribosome moves one codon (3 nucleotides) toward the 3’ end of mRNA, thus shifting previous A-site tRNA to P-site, and opening A-site
  • tRNA with anticodon complementary to A-site mRNA codon binds to ribosomal A-site, with appropriate amino acid attached to tRNA 3’ terminal
  • enzymes in ribosome catalyze formation of peptide bond between 2nd and 3rd amino acids
  • P site tRNA, now separated from its amino acid, exits ribosome
  • ribosome moves one codon (3 nucleotides) toward the 3’ end of mRNA, thus shifting previous A-site tRNA to P-site, and opening A-site
  • repetition of process until stop codon is reached

3. Disassembly of the components follows termination of translation.

  • when ribosomal A-site reaches a stop codon, no tRNA has a complementary anticodon
    • there are three stop codons in the genetic code none of these have a corresponding tRNA
    • when a ribosome encounters a stop codon, a release factor binds to the stop codon

    4. Free ribosomes synthesize proteins for use primarily within the cell b ound ribosomes synthesize proteins primarily for secretion or for use in lysosomes.

    Ribosomes are composed of rRNA and protein.

    • protein (40% of the weight) and rRNA (60% of weight) composition:
    • large and small subunits
    • three tRNA binding sites: E-site, P-site, A-site
    • mRNA binding site: on small ribosomal subunit

    • free ribosomes synthesize proteins for use primarily within the cell itself
    • that bound ribosomes synthesize proteins primarily for secretion or for lysosomes

    Skill: Identification of polysomes in electron micrographs of prokaryotes and eukaryotes.

    polysomes : several to many ribosomes translating the same mRNA into protein each moving in the 5’ to 3’ direction

    6. The sequence and number of amino acids in the polypeptide is the primary structure.

    polypeptide primary structure:

    • sequence and number of amino acids
      • each position occupied by one of 20 amino acids
      • linked by peptide bonds

      7. The secondary structure is the formation of alpha helices and beta pleated sheets stabilized by hydrogen bonding.

      • weak hydrogen bonds between amino and carboxyl groups and different amino acids
        • form at regular intervals, creating a regular structure
        • (not from interactions between variable R- groups)

        8. The tertiary structure is the further folding of the polypeptide stabilised by interactions between R groups.

        • interactions between variable R- groups forming:
          • hydrophobic interactions between nonpolar amino acids
          • hydrogen bonds between polar amino acids
          • ionic bonds between ionic amino acids
          • covalent bonds between sulfur containing amino acids

          9. The quaternary structure exists in proteins with more than one polypeptide chain.


          The word for fish in English and the other Germanic languages (German fisch Gothic fisks) is inherited from Proto-Germanic, and is related to the Latin piscis and Old Irish īasc, though the exact root is unknown some authorities reconstruct an Proto-Indo-European root *peysk-, attested only in Italic, Celtic, and Germanic. [8] [9] [10] [11]

          The English word once had a much broader usage than its current biological meaning. Names such as starfish, jellyfish, shellfish and cuttlefish attest to almost any fully aquatic animal (including whales) once being 'fish'. "Correcting" such names (e.g. to 'sea star') is an attempt to retroactively apply the current meaning of 'fish' to words that were coined when it had a different meaning.

          Fish, as vertebrata, developed as sister of the tunicata. As the tetrapods emerged deep within the fishes group, as sister of the lungfish, characteristics of fish are typically shared by tetrapods, including having vertebrae and a cranium.

          Early fish from the fossil record are represented by a group of small, jawless, armored fish known as ostracoderms. Jawless fish lineages are mostly extinct. An extant clade, the lampreys may approximate ancient pre-jawed fish. The first jaws are found in Placodermi fossils. They lacked distinct teeth, having instead the oral surfaces of their jaw plates modified to serve the various purposes of teeth. The diversity of jawed vertebrates may indicate the evolutionary advantage of a jawed mouth. It is unclear if the advantage of a hinged jaw is greater biting force, improved respiration, or a combination of factors.

          Fish may have evolved from a creature similar to a coral-like sea squirt, whose larvae resemble primitive fish in important ways. The first ancestors of fish may have kept the larval form into adulthood (as some sea squirts do today), although perhaps the reverse is the case.


          Fish are a paraphyletic group: that is, any clade containing all fish also contains the tetrapods, which are not fish. For this reason, groups such as the class Pisces seen in older reference works are no longer used in formal classifications.

          Traditional classification divides fish into three extant classes, and with extinct forms sometimes classified within the tree, sometimes as their own classes: [13] [14]

          • Class Agnatha (jawless fish)
            • Subclass Cyclostomata (hagfish and lampreys)
            • Subclass Ostracodermi (armoured jawless fish) †
            • Subclass Elasmobranchii (sharks and rays)
            • Subclass Holocephali (chimaeras and extinct relatives)
            • Subclass Actinopterygii (ray finned fishes)
            • Subclass Sarcopterygii (fleshy finned fishes, ancestors of tetrapods)

            The above scheme is the one most commonly encountered in non-specialist and general works. Many of the above groups are paraphyletic, in that they have given rise to successive groups: Agnathans are ancestral to Chondrichthyes, who again have given rise to Acanthodiians, the ancestors of Osteichthyes. With the arrival of phylogenetic nomenclature, the fishes has been split up into a more detailed scheme, with the following major groups:

            • Class Myxini (hagfish)
            • Class Pteraspidomorphi † (early jawless fish)
            • Class Thelodonti †
            • Class Anaspida †
            • Class Petromyzontida or Hyperoartia
              • Petromyzontidae (lampreys)
              • (unranked) Galeaspida †
              • (unranked) Pituriaspida †
              • (unranked) Osteostraci †
              • Class Placodermi † (armoured fish)
              • Class Chondrichthyes (cartilaginous fish)
              • Class Acanthodii † (spiny sharks)
              • Superclass Osteichthyes (bony fish)
                • Class Actinopterygii (ray-finned fish)
                  • Subclass Chondrostei
                    • Order Acipenseriformes (sturgeons and paddlefishes)
                    • Order Polypteriformes (reedfishes and bichirs).
                    • Infraclass Holostei (gars and bowfins)
                    • Infraclass Teleostei (many orders of common fish)
                    • Subclass Actinistia (coelacanths)
                    • Subclass Dipnoi (lungfish, sister group to the tetrapods)

                    † – indicates extinct taxon
                    Some palaeontologists contend that because Conodonta are chordates, they are primitive fish. For a fuller treatment of this taxonomy, see the vertebrate article.

                    The position of hagfish in the phylum Chordata is not settled. Phylogenetic research in 1998 and 1999 supported the idea that the hagfish and the lampreys form a natural group, the Cyclostomata, that is a sister group of the Gnathostomata. [15] [16]

                    The various fish groups account for more than half of vertebrate species. As of 2006, [17] there are almost 28,000 known extant species, of which almost 27,000 are bony fish, with 970 sharks, rays, and chimeras and about 108 hagfish and lampreys. A third of these species fall within the nine largest families from largest to smallest, these families are Cyprinidae, Gobiidae, Cichlidae, Characidae, Loricariidae, Balitoridae, Serranidae, Labridae, and Scorpaenidae. About 64 families are monotypic, containing only one species. The final total of extant species may grow to exceed 32,500. [18] Each year, new species are discovered and scientifically described. As of 2016, [19] there are over 32'000 documented species of bony fish and over 1'100 species of cartilaginous fish. Species are lost through extinction (see biodiversity crisis). Recent examples are the Chinese paddlefish or the smooth handfish.


                    The term "fish" most precisely describes any non-tetrapod craniate (i.e. an animal with a skull and in most cases a backbone) that has gills throughout life and whose limbs, if any, are in the shape of fins. [21] Unlike groupings such as birds or mammals, fish are not a single clade but a paraphyletic collection of taxa, including hagfishes, lampreys, sharks and rays, ray-finned fish, coelacanths, and lungfish. [22] [23] Indeed, lungfish and coelacanths are closer relatives of tetrapods (such as mammals, birds, amphibians, etc.) than of other fish such as ray-finned fish or sharks, so the last common ancestor of all fish is also an ancestor to tetrapods. As paraphyletic groups are no longer recognised in modern systematic biology, the use of the term "fish" as a biological group must be avoided.

                    Many types of aquatic animals commonly referred to as "fish" are not fish in the sense given above examples include shellfish, cuttlefish, starfish, crayfish and jellyfish. In earlier times, even biologists did not make a distinction – sixteenth century natural historians classified also seals, whales, amphibians, crocodiles, even hippopotamuses, as well as a host of aquatic invertebrates, as fish. [24] However, according to the definition above, all mammals, including cetaceans like whales and dolphins, are not fish. In some contexts, especially in aquaculture, the true fish are referred to as finfish (or fin fish) to distinguish them from these other animals.

                    A typical fish is ectothermic, has a streamlined body for rapid swimming, extracts oxygen from water using gills or uses an accessory breathing organ to breathe atmospheric oxygen, has two sets of paired fins, usually one or two (rarely three) dorsal fins, an anal fin, and a tail fin, has jaws, has skin that is usually covered with scales, and lays eggs.

                    Each criterion has exceptions. Tuna, swordfish, and some species of sharks show some warm-blooded adaptations – they can heat their bodies significantly above ambient water temperature. [22] Streamlining and swimming performance varies from fish such as tuna, salmon, and jacks that can cover 10–20 body-lengths per second to species such as eels and rays that swim no more than 0.5 body-lengths per second. [25] Many groups of freshwater fish extract oxygen from the air as well as from the water using a variety of different structures. Lungfish have paired lungs similar to those of tetrapods, gouramis have a structure called the labyrinth organ that performs a similar function, while many catfish, such as Corydoras extract oxygen via the intestine or stomach. [26] Body shape and the arrangement of the fins is highly variable, covering such seemingly un-fishlike forms as seahorses, pufferfish, anglerfish, and gulpers. Similarly, the surface of the skin may be naked (as in moray eels), or covered with scales of a variety of different types usually defined as placoid (typical of sharks and rays), cosmoid (fossil lungfish and coelacanths), ganoid (various fossil fish but also living gars and bichirs), cycloid, and ctenoid (these last two are found on most bony fish). [27] There are even fish that live mostly on land or lay their eggs on land near water. [28] Mudskippers feed and interact with one another on mudflats and go underwater to hide in their burrows. [29] A single, undescribed species of Phreatobius, has been called a true "land fish" as this worm-like catfish strictly lives among waterlogged leaf litter. [30] [31] Many species live in underground lakes, underground rivers or aquifers and are popularly known as cavefish. [32]

                    Fish range in size from the huge 16-metre (52 ft) whale shark to the tiny 8-millimetre (0.3 in) stout infantfish.

                    Fish species diversity is roughly divided equally between marine (oceanic) and freshwater ecosystems. Coral reefs in the Indo-Pacific constitute the center of diversity for marine fishes, whereas continental freshwater fishes are most diverse in large river basins of tropical rainforests, especially the Amazon, Congo, and Mekong basins. More than 5,600 fish species inhabit Neotropical freshwaters alone, such that Neotropical fishes represent about 10% of all vertebrate species on the Earth. Exceptionally rich sites in the Amazon basin, such as Cantão State Park, can contain more freshwater fish species than occur in all of Europe. [33]

                    The deepest living fish in the ocean so far found is the Mariana snailfish (Pseudoliparis swirei) which lives at deeps of 8,000 meters (26,200 feet) along the Mariana Trench near Guam. [34]

                    The diversity of living fish (finfish) is unevenly distributed among the various groups, with teleosts making up the bulk of living fishes (96%), and over 50% of all vertebrate species. [19] The following cladogram [35] shows the evolutionary relationships of living fishes with their diversity. [19]

                    The Immune System

                    1. Foreign substance invades the body
                    2. Macrophages consume cells and present anigens (APC = antigen presenting cell)
                    3. Macrophages activate Helper T cells
                    4. Helper T cells active B cells (to make antibodies) and Killer T cells

                    How Do Vaccines Work?

                    Vaccines contained a killed or weakened part of a virus (or other pathogen) to stimulate your immune system to react to the antigen. Once you have antibodies for that microbe, the real one will not make you sick.

                    Do you remember who invented the first vaccine?

                    Why do some people not want to vaccinate their children?

                    Why do some people choose not to get the flu vaccine?

                    Watch the video: X-Com: Ufo Defense - Enemy Unknown Part (January 2022).