General Microbiology Ch. 23 and 24
What are the steps in root nodule formation? Explain nod genes, nod proteins, and nod factors.
1) recognize correct partner by both plant and bacterium, and attachment of the bacterium to the root hairs. 2) secretion of oligosaccharide signaling molecules (Nod factors) by bacterium. 3) bacterial invasion of root hair. 4) movement of bacteria to main root by way of infection thread. 5) formation of modified bacterial cells (bacteroides) within plant cells, development of N2-fixing state, and continued plant and bacterial cell division forming the mature root nodule. Nod genes are rhizobial genes that direct steps in nodulation of a legume, that are believed to have independently emerged through horizontal gene transfer (nod & nif). Rhizobium leguminosarum biovar viciae (nodulates peas) have ten nod genes. The nodABC genes encode proteins that produce lipochitin oligosaccharides (Nod factors), which induce root hair curling and trigger cell division in pea plant to form nodule. Nod factors function as primary rhizobial signalling molecules triggering legumes to develop new plant organs: root nodules-host bacteria as nitrogen-fixing bacteroids. Groups use node genes to encode proteins to modify nod factor backbone to form species specific molecule. In R. leguminosarum biovar viciae, nodD encodes positive regulatory protein NodD (controls/promotes transcription of nod genes). NodD inducers are plant flavonoids (organic molecules widely secreted by plants). Some flavonoids are structurally very closely related to nodD inducers in R. leguminosarum biovar viciae and can inhibit nod gene expression in other rhizobial species, indicating legume symbioses is controlled by chemistry of flavonoids secreted by each species of legume. Nitrogenase from bacteroids show same biochemical properties as enzyme from free-living N2-fixing bacteria, including O2 sensitivity and ability to reduce acetylene and N2 (N2 fixation is catalyzed by nitrogenase). Bacteroids are dependent on plant for electron donor for N2 fixation. The major compounds transported across symbiosome membrane and into the bacteroid proper are citric acid cycle intermediates (C4 organic acids: succinate, malate, fumarate). These are used as electron donors for ATP production and, following conversion to pyruvate, as the ultimate source of electrons for reduction of N2. Ammonia produces from N2 fixation is mostly assimilated by the plant by forming organic nitrogen compounds. NH3-assimilating enzyme glutamine synthetase present in high levels in plant cell cytoplasm, it converts glutamate and NH3 into glutamine (glutamine transports bacterially fixed nitrogen throughout plant.
Examples of microbe-fungi interactions (lichens): What happens between the two organisms? How do each one benefit? Are there key organisms (think names) that form these symbioses?
Anabaena or Nostoc are nitrogen-fixing cyanobacteria when partnered with lichens. In few lichens, 2 phototrophic species are in 1 thallus, as well as additional low-abundance photobiont species. Variation of lichen structure is determined by fungus. More that 18,000 fungi species can form lichen associations with variety of photobionts. Habitat range from tropical to polar climatic zones, costal to high altitude habitats. Lichens usually grow slowly, depending on organisms in symbiosis, temperature, rainfall, sunlight received. Limited diversity of photobionts (lower than fungi), resulting in many lichens having same phototrophic partner. Partner photobiont is determined by lichen reproduction (asexual preserves specific symbiotic association via fungal propagules dispersal (results in less adaptive flexibility), sexual releases fungal spores which lack photobiont and require independent acquisition of new symbiotic partner after dispersal-allows fungus to form new symbiotic association with locally adaptive features. Lichens may also have more than one fungus and also host bacteria that may benefit association. Cortex in lichens consists of fungal structural tissue bounding the phototroph layer, it can contain yeast (basidiomycete) in addition to ascomycete. Many lichens associate with alphaproteobacteria (order Rhizobiales) that fix nitrogen to symbiosis similar to cyanobacteria. Lichen symbiosis produces vitamins, protection from toxic compounds (ex. lichens inhabiting arsenic contaminated environments increased abundance of genes encoding arsenic resistance)
How many microbes inhabit our body? How does this compare to our number of cells?
Around 10^13 cells in human microbiome, which is the about the same as the number of human cells in a single person.
What are the key organisms of the skin, mouth, stomach, and digestive tract? What microbial processes/metabolisms dominant in the gut? What drives the changes we see during the transition from habitat to habitat?
At each site, one group of bacteria dominates, and the dominant group is different at each site. The diversity of gram-positive bacteria is greatest on the surface of the skin and urogenital tract, while diversity of gram-negative bacteria is greatest in the gastrointestinal tract. Gastrointestinal tract includes stomach, large and small intestine, digests food and absorbs nutrients-many nutrients produced by naturally originating microbiota, and it's mostly bacteria. Acid tolerant bacterium Helicobacter pylori colonizes stomachs in 50% of humans, discovery of this informed us that the stomach isn't sterile. Stomach has low pH (1-2) and microbial diversity (dominated by Firmicutes, Bacteroidetes, actinobacteria in gastric fluids, and Firmicutes and proteobacteria in mucosal lining). H. pylori can cause upper gastrointestinal disease. Small intestine is lower in pH (~4-5) and has low microbial diversity. Duodenum is very acidic and resembles stomach communities. Ileum has slightly higher pH, so less acidic and higher bacterial numbers (lower ileum has 10^5-10^7 cells), but more anoxic. Fusiform anaerobic bacteria typically present (one end connected to intestinal wall), and colonic microbiota is largely supported by degradation of complex indigestible carbohydrates-necessary for small intestine since it competes with host for rapid uptake of small carbohydrates, and needs bacteria that can live with or without complex indigestible carbohydrates. Mouth secretes mucin to retain moisture and inhibit microbial attachment, but some adhere to epithelial surface and colonize it, causing growth of normal microbiota or microbial disease. Saliva contains antibacterial substances, but accumulation of food particles and cell debris causes high concentration near teeth and gums contributing to damage and disease (occurs when mutualisms are unstable). Skin has microenvironments of varying temperature, pH moisture, sebum content (oil), surface characteristics. Moist sites dominated by staphylococci, Oily/fatty areas (sebaceous areas) dominated by Propionibacterium-colonizes follicular sebaceous gland system and hydrolyzes triglycerides in sebum causing release of free fatty acids that promote adherence of bacterium which can cause acne. Propionibacterium on head, face, upper back, upper chest, while Staphylococcus on groin, armpit, toe web (areas higher in temp and moisture content).
What constitutes a coral and why are corals dying (bleaching)?
Coral reef ecosystems are products of mutualistic associations between microscopic phototrophs and simple marine animals. Chlorella is green algae symbiont that associates with sponges and freshwater hydras. Staghorn coral symbiosis between stony corals (phylum Cnidaria) and Symbiodinium. Symbiodinium symbiont is distributed throughout the coral skeleton in coral tissue. Stony corals have ectoderm and gastroderm layers that harbor dinoflagellate (genus of Symbiodinium) symbiont intracellularly in membrane-bound vesicles (symbiosomes) within cells of inner gastrodermal tissue layer. Coral symbiosomes are analogous to bacteroid-filled vesicles that develop in plant cells of legume root nodules. Coral skeleton is light-gathering structure that highly enhances light by harvesting Symbiodinium cells to maintain symbiosis. *Coral is threatened with extinction mostly due to humans. Ongoing loss of coral ecosystems is thought to be the result of elevated atmospheric CO2: increased sea surface temperature, rising sea levels, ocean acidification. Coral have loss of structure from reduced calcification caused by acidification and bleaching. Coral bleaching is loss of color from host tissues caused by lysis or expulsion of pigmented Symbiodinium symbionts (within tissues), revealing the underlying white limestone skeleton. Bleaching is caused by increased sea surface temperature and irradiance. High temp and irradiance impair photosynthetic apparatus of dinoflagellates, resulting in production of reactive oxygen species (ex. singlet oxygen and superoxide) that damage host and symbiont. Bleaching thought to be caused by protective immune response of host that destroys compromised symbionts. 0.5 to 1.5 degrees C above local maximum temp for several weeks can cause rapid bleaching. This thermal stress on coral shows evidence of climate change and microbe ecosystem response to change. In coral-Symbiodinium symbiont mutualism, thermal tolerance is benefited by Symbiodinium, and after bleaching, the mutualism can shift to a more thermally tolerant symbiont. Many Symbiodinium species have different thermal tolerance. When coral is bleached, a more heat-tolerant symbiont can replace the bleached species (symbiont swapping), where species shift results from the more robust growth of a more heat-tolerant cariant already associated with coral but in very low numbers; variant then thrives following loss of original symbiont and bleaching event. Predicting environmental stress from symbiont species can help predict future health of corals and their symbionts.
What are examples of Dysbiosis? Do fecal transplants work?
Dysbiosis: an altercation or imbalance of an individual's microbe relative to normal, healthy state, primarily observed in the microbiota of digestive tract or skin. Typified by increased numbers of facultative aerobes (Enterobacteriaceae) and chronic inflammation. These physiological changes play important roles in development of inflammatory bowel disease and obesity. Examples of Dysbiosis: gut microbiota in inflammatory bowel disease, oral cavity dental caries where bacteria attach to solid surfaces and cause cavities and gum disease, dysbiosis of normal vaginal microbiota associated with inflammatory infection (vaginitis) or less severe (vaginosis) caused by overgrowth of yeast Candida or STDs, necrotizing enterocolitis (NEC) in premature infants where normal sequence of gut colonization is disrupted, Sepsis induces alterations in gut microbiota composition. Fecal transplant Antibiotics kill or inhibit some normal microbiota and the targeted pathogen, leads to significant loss of normal gut microbiota. Antibiotic exposure during first three months of life can disrupt microbiota that influence host energy metabolism, causing increased weight gain, child autoimmune disorders, disruption of normal development of human gut microbiota. With Clostridioides difficile infections, antibiotic-resistant opportunistic pathogens become established in young children or elderly following antibiotic treatment that disrupts normal microbiota, and C. diff is complication of antibiotic therapy where infection with toxigenic Clostridioides difficile and inability to resolve infection with repeated follow-on administrations of antibiotics occurs. Symptoms of C. diff infection are mild diarrhea to severe abdominal pain and fever, with inflammatory lesions and bowel perforation (can cause septic shock and death. Fecal transplants can treat C. diff, where fecal material from gut of healthy donor into gut of infected patient results in restoring a healthy colon. Fecal transplants reintroduce normal microbiota into gut of someone with intestinal disease of bacterial origin and have transplanted microbial community become established and exclude disease-causing organisms. 90% patients recover without relapse with transplant, where only 25% with standard antibiotic treatment. Fecal transplants can alleviate forms of metabolic syndrome (elevated blood pressure and glucose levels, excess belly fat, abnormal cholesterol levels (presurser of type 2 diabetes). Metabolic syndrome patients receiving fecal transplant from lean healthy donor had significantly increased insulin sensitivity, increased fecal levels of butyrate, greater gut microbial diversity, increased abundance of bacterium that produces butyrate.
Examples of microbe-animal interactions (Rumen): What happens between the two organisms? How do each one benefit? Are there key organisms (think names) that form these symbioses?
Earth's dominant herbivores (cows, sheep, goats, deer, etc) are ruminant mammals have special foregut digestive organ (rumen) where microbes digest cellulose and other plant polysaccharides. Human food economy depends on ruminant animals, so rumen microbiology is very important. Rumen is very large (holds 100-150 liters in cow, 6 in sheep), its position is before the stomach. Rumen constant temp (39 C), narrow pH (5.5-7), depending on when animal last fed, and anoxic environment are important factors in rumen function. Fistula implant used to easily remove samples to study microbes and digestion. Food remains in rumen for 20-50 hours depending on feeding schedule and other factors. During this time, cellulolytic microbes hydrolyze cellulose (frees glucose), Then glucose undergoes bacterial fermentation with production of volatile fatty acids (VFAs)-acetic, propionic, butyric acids. VFAs pass through animal as main source of energy, gaseous fermentation products carbon dioxide and methane are released by eructation (belching). Bacteria adhere to food particles which go through gastrointestinal tract and then to digestive processes. Bacterial cells that digested plant fiber in rumen are then digested in acidic abomasum. Bacteria in rumen biosynthesize amino acids and vitamins, and they are major source of protein and vitamins for animal. Rumen contains bacteria, archaea, fungi, and nonphototrophic protists. Anaerobic bacteria and archaea dominate rumen because of its strictly anoxic compartment, where some anaerobic microbial eukaryotes are present. Cellulose is converted to fatty acids, carbon dioxide and methane in multistep microbial food chain. Rumen contains 300-400 bacterial species, Firmicutes and Bacteroidetes dominate bacterial diversity in rumen, while methanogens make up entire archaeal population. Various rumen bacteria hydrolyze cellulose sugars and ferment sugars to VFAs (Fibrobacter succinogenes, Ruminococcus albus) Fibrobacter produce enzymes on outer membrane, Ruminococcus produces cellulose-degrading protein complex bound to cell wall. Both need to bind to cellulose particles to degrade them.
How does diet affect your gut microbiome? hooked on a *gut* feeling! High for no reason!
Healthy homeostasis is when gut microbial community is stable and resilient. Healthy gut microbiota is based on dietary, metabolic, immunological. Diet is critical determinant of homeostasis- short-chain fatty acids. Among SCFAs, butyrate serves a critical function in controlling immune surveillance and metabolism of colonocytes-absorb epithelial cells of large intestine. Butyrate activates process that maintains anoxic environment near epithelial surface that is favorable to obligately anaerobic bacteria that produce butyrate. If butyrate-producing microbes are depressed by dramatic diet change or antibiotic treatment, colonocyte metabolism is shifted towards glucose fermentation and lower oxygen consumption, resulting in greater passage of oxygen and proliferation of facultatively aerobic bacteria that invoke inflammatory response. Trimethylamine oxide (TMAO) in liver contributes to coronary thrombosis by increasing blood platelet hyperresponsiveness. Increase of trimethylamine (TMA) ,that is converted to TMAO in liver, can cause cardiovascular disease (CVD), accelerated atherosclerosis (clogging and stiffening of arteries) in mice and is correlated with higher incidence of CVD in humans. Plant rich diets (high fiber) work against development of these pathologies, why eating fiber rich diet and carbohydrate-based fermentation in healthy gut is important.
Gut Microbiomes: What is exchanged how do microbes in the gut help the organism? What are examples of termites and rumen bearing organisms (fore vs. hind gut)?
Herbivorous mammals have foregut and hindgut digestive patterns. Foregut fermentation, the microbial fermentation chamber precedes the small intestine, originated in ruminants (cattle, sheep, monkeys, sloths), where ingested nutrients are degraded by gut microbiota before reaching acidic stomach and small intestine. Foregut have advantage over hindgut in that cellulolytic microbial community of foregut passes through acidic stomach, during which microbial cells are killed by acidity and become protein source for animal. While in hindgut fermenters (horses and rabbits), the remains of the cellulolytic community pass out of animal in feces because of its position posterior to acidic stomach; because of this, many hindgut fermenters like rabbits eat their own feces (coprophagy) in order to recover protein from microbial cells. Hindgut fermenters, horses and rabbits, have one stomach but use cecum digestive organ located between small and large intestines as their fermentation vessel. Cecum contains fiber- and cellulose-digesting (cellulolytic) microorganisms. Mammals (like rabbits) rely on microbial breakdown of plant fiber in cecum (cecal fermenters), while other hindgut fermenters use cecum and colon to breakdown fiber via microbes. Rumen digestive organ Earth's dominant herbivores (cows, sheep, goats, deer, etc) are ruminant mammals have special foregut digestive organ (rumen) where microbes digest cellulose and other plant polysaccharides. Human food economy depends on ruminant animals, so rumen microbiology is very important. Rumen is very large (holds 100-150 liters in cow, 6 in sheep), its position is before the stomach. Rumen constant temp (39 C), narrow pH (5.5-7), depending on when animal last fed, and anoxic environment
How does the large intestine stay anoxic? Key organisms? or things produced by the body?
In large intestine, colon have large amount of bacteria, and some individuals have archaea (methanogens), it's a fermentation vessel where microbiota use nutrients from digesting food. Facultative aerobes (E. coli) present in few numbers since obligate anaerobes predominate. Facultative aerobes consume traces of oxygen in colon, making large intestine strictly anoxic. Anoxia promotes growth of obligate anaerobes (Clostridium, Bacteroides-99% of all prokaryotic cells). Bacteria are dominant population (10^10-10^11 bacterial cells of fecal contents-bacteria compose 1/3 of fecal matter weight). Organisms in lumen are continuously displaced downwards by flow of material- bacteria lost are replaced by new growth. Passage of material through GI tract is 24 hours, growth rate of bacteria- 1-2 doublings per day. Human sheds 10^13 bacterial cells each day in feces. Inner mucus layer ( made of mucin secretion-produced by goblet cells) of large intestine protects organ and rarely has bacteria, goblet cells produce antimicrobial peptides that prevent microbial contact with epithelium. 2 families dominate gut: Firmicutes (Lachnospiraceae and Ruminococcaceae)- digest polysaccharide polymers in plant fiber (cellulose, pectin) and ferment into short fatty acid chains; and bacteroidetes (bacteroidaceae- further degrade glycoproteins within mucus layer, suggesting larger role during times of food stress).
How does the microbiome affect obesity?
Initial evidence that microbes affect obesity: 2 groups of mice were fed same food, 1 group was microbe-free and other was normal/ Normal mice had 40% more body fat than microbe-free/germ-free mice. Germ-free mice were inoculated with fecal transplant from normal mouse and they developed gut microbiota and their body fat increased, although no food change occured. Mice experiment showed colonization triggers expression of host genes for glucose uptake and lipid absorption and transport in ileum (small intestine), indicating a link between gut microbial composition and ability of host to harvest energy from diet, contributing to obesity. It was hypothesized that methanogens increase efficiency of microbial conversion of fermentable substrates to volatile fatty acids (VFAs) by consuming hydrogen (like what occurs in rumen), making more VFAs available for absorption by mouse. In non-obese mouse, fewer hydrogen consuming methanogens are present, making fewer VFAs from Firmicutes fermentation available to the mouse. We don't know what triggers difference in methanogen content of lean vs obese mice. When human twins (one obese, one lean) feces was transplanted into germ-free mice with same diet, the obese twin feces made obese mice gain significantly more weight compared to lean mice receiving obese twin feces. So, specific but widely distributed gut microbes exist that can control an animal's metabolism to yield a lean or obese body type.
Examples of microbe-fungi interactions (lichens): What happens between the two organisms? How do each one benefit? Are there key organisms (think names) that form these symbioses?
Lichen (one/two species of fungi in symbiotic relationship with an alga or cyanobacterium-usually nitrogen fixing) symbiosis originates from ancient mutualistic association. The alga/cyanobacterium (phototrophic) produces organic matter that feeds the fungus, produces photobiont cells that are embedded in layers/clumps among the fungus cells (together forming thallus) which protects from erosion by rain/wind. The fungus (chemotroph) provides firm anchor for phototrophic partner to grow, releases lichen acids (promote dissolution & chelation of inorganic nutrients from surface its on, needed for phototroph), facilitates uptake of water & sequesters some for phototroph (allows lichens to colonize in arid environments)
Examples of microbe-microbe interactions (heterotroph and chemolithoautotroph): What happens between the two organisms? How do each one benefit? Are there key organisms (think names) that form these symbioses?
Microbe-microbe interaction example: mobile heterotroph and a sulfur oxidizing phototroph (chloroflexi) ~ heterotroph gains carbon and in return keeps the sulfur oxidizer in an anoxic zone
What are the life stages, and how do they affect your gut? How does your microbiome develop? Is it tied to diet?
Microbiome stabilizes with age, due to more exposure and as immune system develops. Less microbes when we are younger, microbiome expands with age
microbiota and microbiome
Microbiota-types of organisms present in specific regions of the body Microbiome- a functional collection of different microbes in an environmental system such as the human body
Examples of microbe-plant interactions (legumes): What happens between the two organisms? How do each one benefit? Are there key organisms (think names) that form these symbioses? What are the key factors involved in plant-microbe symbiosis initiation? - nodule formation-
Most mutualisms between plants and microbes increase nutrient availability to plants or defend plants against pathogens. 3 types of symbiosis: 1) mutualism where nature of symbiosis is understood in detail (root nodules), 2) mutualism where plants expand and interconnect root system through association with fungus (mycorrhizae), 3) symbiosis that's harmful to plant (crown gall disease). Legumes are flowering plants that bear seeds in pods and are agriculturally important for human/animal food, save farmers money (reduces fertilizer & pollution) since they don't require nitrogen. Symbiosis between leguminous plants and nitrogen-fixing bacteria (rhizobia of alpha or betaproteobacteria) grow in soil or infect leguminous plants to establish symbiotic relationship. Same bacterial genus or even species of legume can contain both rhizobial and nonrhizobial strains of N-fixers. Root nodules form when rhizobia infects legume roots, resulting in bacteria converting N2 to NH3, and they increase fixed nitrogen content of soil (nodulated legumes grow well on unfertilized nitrogen deficient soil, while other plants grow poorly. Legume can't fix N2 without bacterial symbiont, but rhizobia can in pure culture. Interaction of plant and bacterial partner induce production of an iron-containing and O2-binding protein (leghemoglobin) in healthy N2-fixing nodules. Leghemoglobin controls O2 levels in nodule, it acts as oxygen buffer cycling between oxidized and reduced iron to supply O2 for bacterial respiration while keeping unbound O2 low in nodule (in nodule, 10,000 leghemoglobin-bound O2 : 1 free O2). Cross-inoculation group is a group of related legumes that can be infected by a particular rhizobial species, and they develop leghemoglobin-rich N2-fixing nodules when inoculated/infected with correct rhizobia strain obtained from other legume within group. The roots of leguminous plants secrete organic compounds that stimulate growth of a diverse rhizosphere microbial community. If rhizobia of correct cross-inoculation group are in the soil, they will form large populations and eventually attach to root hairs extending from plant roots. Adhesion protein (rhicadhesin) on cell surface of rhizobia, lectins and specific receptors in plant cytoplasmic membrane aid in attachment. After attachment, rhizobial cell penetrates into root hair (causes curling from Nod factors secreted by bacterium), bacterium induces plant to form infection thread (cellulosic tube) that spreads infection down root hair, and plant cell division forms tumor-like nodules (plant cells and bacteroides). Aquatic/semi aquatic tropical legumes enter plant at loose cellular junctions of roots emerging perpendicular from established root (lateral roots) or stem in water, where some rhizobia develop infection threads and others don't. Stem-Nodulating Rhizobia form N2-fixing nodules on the submerged portion their stems rather than their roots. In tropical regions with nitrogen deficient soil.
Examples of each kind of symbiosis
Mutualism symbiosis: "Chlorochromatium aggregatum"-consortium association develops between nonmotile green sulfur bacteria (obligately anaerobic phototrophs of Chlorobi phylum of betaproteobacteria) and motile nonphototrophic bacteria in freshwater. The basis of the mutualism of these consortia is in the phototrophic production of organic matter by the green sulfur bacterium and the motility and organic matter consumption of the chemotrophic partner organism. The consortium consists of 13-69 green sulfur bacteria (epibionts) that surround and attach to central, colorless, flagellated, rod-shaped bacterium. The central bacterium in "Chlorochromatium aggregatum" is surrounded by rod-shaped green bacteria, where other species have brown epibiont, and another has green epibionts w/ gas vesicles. Green and brown sulfur bacteria differ in types of bacteriochlorophyll and carotenoids they contain, both inhabit stratified lakes where light penetrates to depths where water contains hydrogen sulfide (primary electron donor for photosynthetic CO2 fixation by phototroph. In stratified lakes, the motile consortia reposition rapidly to remain in regions where conditions are favorable for photosynthesis. Motile consortia move up and down in the water column much faster than free-living green sulfur bacteria because of their small size, which takes much more time to move via buoyancy from gas vesicles (can't change position fast enough during day). Epibionts in neighboring lakes have identical 16S rRNA gene sequences, but similar epibionts in widely separated lakes differ. "Chlorochromatium aggregatum" requires alpha-ketoglutarate for growth (supplied by epibiont), central cell only assimilates fixed carbon in presence of light and sulfide (active epibionts transfer nutrients to central bacterium), central bacterium has mad massive gene loss, so it can't grow without green sulfur bacterium. Phototroph feeds nutrients to chemotroph, chemotroph dependent on phototroph partner via fusion of tubular extensions of central bacterium's periplasm to epibiont in common periplasmic space. -Methanotrophic consortia that oxidize methane to CO2 in anoxic marine sediments. Methanotrophic archaea from associations with sulfate-reducing bacteria for anoxic hydrocarbon oxidations, oxidation of methane and short-chain alkanes, direct interspecies electron transfer (DIET). Symbiotic associations between microorganisms and plants can be mutualistic, where the microbe and the plant exchange nutrients.
Examples of fungi-plant interactions (mycorrhizae): What happens between the two organisms? How do each one benefit? Are there key organisms (think names) that form these symbioses? What are the key factors involved in plant-fungi symbiosis initiation?
Mycorrhizae are mutualisms between plant roots and fungi in which nutrients are transferred in both directions. The fungus transfers inorganic nutrients (phosphorus, nitrogen) from soil to plant, and the plant transfers carbohydrates to fungus (mutualistic symbiosis in agricultural applications- both benefit). In ectomycorrhizae, fungal cells form an extensive sheath (fungal mantle) around outside of root with slight penetration into the root cellular structure. As rootlets emerge, they are rapidly colonized by the fungi. They are typically found on long and short roots in forests trees (mycorrhizal trees). Ectomycorrhizal hyphae extending from fungal mantel and penetrating between epidermal and cortical cells form Hartig net network where nutrient exchange between fungus and host plant occurs that benefit plant. Most fungi don't catabolize cellulose or leaf litter polymers, but do catobilize simple carbohydrates and typically have one or more vitamin requirements. They obtain carbon from root secretions and obtain inorganic minerals from soil. Mycorrhizal fungi are most likely obligate symbionts. Nutrient transfer from well-illuminates overstory plants to shaded trees is thought to help equalize resource availability, subsidizing young trees and increasing biodiversity by promoting coexistence of different species. In endomycorrhizae, part of fungus is deeply embedded within cells compromising root tissue. Greater diversity than ectomycorrhizae. Most are arbuscular (little tree) mycorrhizae (AM) that comprise a phylogenetically distinct fungal division (Glomeromycota-possible ancestral type, 450 million years ago, important evolutionary step in successful invasion of dry land by terrestrial plants), of which all or most species are obligate plant mutualists. AM colonize 70-90% of all terrestrial plants, they produce lipochitin oligosaccharide signaling factors (Myc factors) closely related to Nod factors in rhizobium legume symbiosis, and myc factors initiate formation of mycorrhizal state. AM root colonization begins with germination of soilborne spore, producing branched germination mycelium that recognizes host plant through reciprocal chemical signalling. AM spore germination and mycelial branching induced by strigolactones, plant hormones released by roots that factor into plant development. Hormone represses above ground growth when plant is nutrient-limited and stimulates root system growth, enhancing production of lateral roots and root hairs (stores nutrients for later use above ground). Myc factor produced by AM fungal mycelium signals plant to initiate developmental process, then fungus forms contact structure (hyphopodium) with root epidermal cells, then hyphae extend into plant from hyphodiums, then form branched/coiled hyphal structures (arbuscules) in plant inner cortex cells, near vascular tissues., remaining separated from plant protoplasm by apoplast region-increases area between plant and fungus. Then inorganic nitrogen and phosphorus are mined from soil by fungi, converted to arginine and polyphosphate, and translocated through hyphae to plant. Plant benefits when it absorbs nutrients from environment more efficiently because of fungus increasing surface area, branching roots to more nutrients (competitive advantage) and supporting plant diversity, and fungus benefits from steady supply of organic nutrients from plant.
What is probiotic vs prebiotic? How do they work?
Probiotics: a live microorganism, when administered in adequate amounts, confers a health benefit on the host. Bifidobacterium and Lactobacillus bacteria are most common. They are usually delivered to the gastrointestinal system by ingestion of fermented milk product (yogurt) with hope to suppress gut ot urogenital disturbances. Most scientists say it has little therapeutic value, but human microbiome research, but success of fecal transplants points to therapeutic potential of modification of gut microbiome, but there is minimal understanding of mechanisms behind successes and why they don't work in some cases. Accidental ingestion of a Bacillus strain prevented colonization by pathogenic Staphylococcus aureus. Bacillus prevents colonization of S. aureus by interfering with the S. aureus quorum-sensing signaling system. ultimately preventing transcription of genes encoding virulence; this strain can be marketed as an effective probiotic to eliminate intestinal and nasal S. aureus colonization (important since S. aureus infections are difficult to treat because of prevalence of multi-antibiotic-resistant strains, and it's better to use probiotic than antibiotics that can affect gut microbiome). Probiotics are effective in reducing incidence of necrotizing enterocolitis (NEC)-severe inflammatory injury to intestine of premature infants where 1/4 infected infants die. Prebiotics: food additive that promotes growth and activity of beneficial microorganisms, usually in gastrointestinal tract. Prebiotics promote ingestion of certain nutrients as microbial growth stimulants with idea that they will nurture particular bacterial species already present in gut and known to be associated with a healthy colon. Prebiotics are typically carbohydrates that are indigestible by the body but are a source of carbon and energy sources for certain fermentative gut bacteria. Fructooligosaccharides (complex sugars) stimulate desirable gut microbes, inulin (complex polysaccharide) is promoted as major prebiotic. Some probiotics contain prebiotics (some yogurts) to supply both beneficial aspects in single treatment (synbiotics are both). Synbiotics have been used to treat sepsis in young children/infants (systemic infection from inflammation of gut)
What kinds of metabolites are produced by our microbiome?
Products of intestinal microbiota-volatile fatty acids, hydrogen, carbon dioxide, methane, other substances and nutrients, vitamins B12 and K, amino acids that humans can't make-made my microbiota and absorbed in colon, steroids-modified in intestine by microbiota and absorbed in gut. Microbial metabolites also generated in gut-peptides that secure colonization of producing organism by inhibiting organisms closely related to producer. Gut bacteria can synthesize high levels of metabolites derived from reduction of amino acids (tryptamine-neurotransmitter, 4-ethylphenylsulfate).
What is the role of SCFA/SCVAs in gut health?
Short-chain fatty acids (SCFAs; primarily butyrate, propionate, acetate) produced by fermentation of fiber by gut microbiota serve central role in development and maintenance of healthy gut. SCFAs are an important energy source for intestinal cells, and function as signalling molecules to regulate cellular metabolism and immune surveillance. Binding SCFAs to specific intestinal cell surface receptors regulates cellular metabolism, increases secretion of antimicrobial peptides (defensins), elevates production of hormones affecting energy recovery and sensations of hunger, has dampening effect on inflammatory response through regulatory T cell (Treg) signalling system. SCFA signalling promotes tight junction formation, which could contribute to leaky gut system if PPAR-y activity is depressed. Disruption of tight junctions leads to greater exposure to gut microbiota, resulting in inflammatory response (dysbiosis).
Bioluminescence: How do bacteria talk to each other? What gene system is involved with light production, what is the key enzyme?
Some Gammaproteobacteria (vibrio, Aliivibrio, Shewanella, Photorhabdus) emit light (bioluminescence), most inhabit marine environment, some colonize light organs of certain marine animals to allow animal to signal, avoid predators, and attract prey. Some isolates are facultative aerobes (need O2 for bioluminescent). Luminescence in bacteria require luxCDABE gene catalyzed by luciferase enzyme (uses O2, RCHO, and FMNH2 as substrates), transcribed by LuxR regulatory protein and induced by acyl homoserine lactone (AHL) in high population density (autoinduction). AHL accumulates in high density and when it reaches certain concentration in cell AHL is bound by LuxR to form complex that activates transcription of luxCDABE, then cells become luminous (The lux operon is expressed and the bacteria now can create light). Build up of AHL overtime due to population growth can inform microbe cell about population size. As cell densities increase, the lux operon which is repressed at low densities, is induced by the presence of the AHL through a signalling cascade. Genes are turned on through quorum sensing- ensures luminescence develops only at high population density to allow light produced to be visible to animals. Then the animals feed on luminous material and bring bacteria into animals gut to grow. Luminous material may also function as light source in symbiotic light organ associations. Quorum sensing regulates and controls activities (produces extracellular enzymes, expression of virulence factors-high population density is beneficial if bacteria are to have biological effect). Bobtail squid: Many higher organisms that create symbiosis with bioluminescent bacteria have specialized organs for microbes to stay in. Bobtail squid hunts at night and uses light organ that resembles moonlight penetrating marine waters for camouflage, it will empty the specialized light organ in the morning and regrow a population of Vibrio during the day. Endosymbiont is derived from background seawater. HORIZONTAL GENE TRANSFER used to get symbiont from environment. Bioluminescence and carbon cycle: Through feeding dynamics and biological carbon pump, luminescent bacteria are dispersed throughout ocean. Uptake and concentration of microbes on particles could give rise to glowing food sources for copepods etc in the dark ocean.
Name of partners in a symbiosis
Symbionts
Endosymbionts of insects (mutualism): How are they transferred? What are there specialized organs? What's there basic genome information for what happens (like genome reductions)
Symbiosis between microbes and insects provide nutrient advantages or protection from parasites in insects. Endosymbionts are intracellular bacteria, usually in specialized organs of insects. Transfer of microbial symbionts can be horizontal transmission (less specificity) or heritable/vertical transmission (focus on vertical). All heritable microbial symbionts lack free-living replicative stage (obligate symbionts), most require host for replication. Heritable symbionts are primary (required for host reproduction, restricted to bacteriome containing bacteriocytes cells) or secondary (not required for host reproduction, not present in all within a species, not restricted to particular host tissue). Secondary invade different cell types, can live extracellularly in insects hemolymph fluid cavity. Examples: Whiteflies infected with Rickettsia produce offspring faster and offspring live longer than in uninfected flies, A Spiroplasma species protects insect from parasitic nematode worm, symbiotic Wolbachia infect 60-70% of all insect species which affects male insect sperm that sterilizes uninfected females. Most aphids harbor Buchnera in their bacteriomes, which have genes encoding the biosynthesis of 9 amino acids missing from the sap. Symbiont-free aphisa require all amino acids in diet which is not in the sap. Certain amino acid synthesis synergy between symbiont and host-Buchnera lacks required enzyme for leucine biosynthesis, but is provided in aphid's genome. Extreme genome reduction occurs in primary insect symbionts (high adenine and thymine, accelerated rates of mutation). Most insect symbiont genomes are small (results in fewer DNA repair enzymes), where free-living bacteria genomes are much larger and 50% G + C base composition. Tremblaya princeps is among smallest genome known for any cell. Two types of spontaneous mutations: cytosine deamination and oxidation of guanosine (change GC to AT if not repaired). Insect symbionts retain genes needed for host fitness and molecular processes (transcription, translation, replication), and lost genes indicate dependence on host for lost genes/functions. The insect symbiont provides biosynthetic nutrients to host, while pathogen obtains biosynthesis nutrients from host. Horizontal gene transfer is the movement of genetic information across normal mating barriers. This is usually rare between insect symbiont and host genomes, but can have movement of genetic info between symbionts with specific insect host. Rove beetle (paederus beetle) deters predators with chemical pederin (from horizontal gene transfer) synthesized by endosymbiotic Pseudomonas species, chemical accumulates in insects hemolymph and deposits into eggs, crushing beetle can cause skin illness from chemical. Leafcutter ants (attine ants) have symbiotic association between four microbial symbionts (small parasitic fungus on cultivated fungus, N-fixing bacteria associated with cultivated fungus, actinobacterium that recognizes parasitic fungus, black yeast that interferes with actinobacterium) and insect, establishing obligate mutualism with fungus using small leaf fragments to feed fungus. Ant colony-founding queens vertically transmit fungus pellet between generations and establishes new cultivated fungus nest. N-fixers (Klebsiella, Pantoea) associated with fungus enrich nutrition by adding nitrogen to nitrogen poor leaf growth substitute. Ant forms symbiosis with actinobacterium (pseudonocardia) that inhibits growth of parasitic Escovopsis fungus to protect cultivated fungus. Black yeast steals nutrients from Pseudonocardia, reducing ability to suppress Escovopsis growth. Ant has symbiosis with fungi and bacteria. Bees have only five dominant bacterial species in gut which affects their protection against environmental stressors/pathogens. Coevolution of genome caused different bacterial species strains to become host-specific (S. alvi colonizes honeybees but not bumble bees). Gut microbes carry genes for using uncommon toxic sugars that are normally harmful to bees, protecting them. Microbe defends bee from invasive microbes by stimulating bee to product antimicrobial peptides to target pathogenic bacteria.
Pathogenicity: Host and symbiont team up to kill-nematodes
Two families of nematodes (Heterorhabditidae, Steinernematidae), obligate pathogens of insects and together constitute a group of entomopathogenic (insect-killing) invertebrates that have wide range of insect hosts. Insect lethality results from specific association between nematode and bacterial symbionts, producing insecticidal compounds. Nematodes use compounds produced by bacterial symbiont to kill insect prey. Gram-negative bacteria (Photorhabdus and Xenorhabdus) are primary symbionts of entomopathogenic nematodes. Photorhabdus associate with Heterorhabditidae, and Xenorhabdus associate with Steinernematidae (points to coevolution between nematodes and bacterial symbionts, since various entomopathogenic nematodes have different insect host specificities). Bacteria invade insect's hemocoel (body cavity containing bloodlike hemolymph of circulatory system) through mouth or anus, then bacteria are released from bacterial receptacle (chamber that allows bacteria to grow and protects growth) into hemolymph and grow quickly. Then they stop insects immune system by producing hemolysins, toxins, digestive enzymes that promote release of nutrients from host tissues. Bacterial symbionts produce antibiotics to inhibit microbe competitors. Bacteria and digested host nourish nematodes which slowly kills insects (1-22 days) by depleting nutrients from host and by nematodes producing new infective nonfeeding juveniles that can withstand outside environment to repeat cycle. Nematodes studied for alternative insect pest control.
What was Eukaryogenesis driven by? Process and what became mitochondira.
When eukarya diverged from archaea, symbiosis made it so they could distinguish and separate. First interactions were with sulfate reducing bacteria allowing waste from metabolism to be eaten —> oxidation event —-> engulfment and incorporation of facultative anaerobes Alphaproteobacteria became mitochondria
Mutualistic symbiosis
both partners benefit
What kinds of symbiosis are there?
mutualistic, commensal, parasitic, and pathogenic
Parasitic symbiosis
the host is negatively affected by the microorganism (One symbiotic partner benefits and the other is harmed)
Commensal symbiosis
the host neither benefits nor is harmed by the microorganisms (one symbiotic partner benefits and the other is unaffected)
Microorganisms in the human body
the human microbe is the total complement of microorganisms associated with humans, and these microbes colonize a variety of different habitats in the human body. Each colonized site in the body is characterized by a specific set of physical, chemical, and nutrient conditions selective for particular types of resident or transient microorganisms.
Pathogenic symbiosis
the microorganism causes disease in the host
