Module 5 - Challenging Life Flashcards
Carbon dioxide + temperature of atmosphere
In geological time, carbon dioxide levels and temperature were too low
1000 PPB = cut off for carbon dioxide for plants (now that it is below, it is limiting plants growth)
Increasing atmospheric co2 affects rainfall, diseases and pests, temperature of atmosphere
Plants grow better in higher carbon dioxide levels but also show decrease of nutrients in plants (proteins + nutrient levels)
This is due to more carbon in plants but less N for proteins and other necessary macronutrients for humans
Plant Modifications to changing atmosphere
In C3 plants, organic carbon dioxide is fixed by Rubisco to form a C6 compound
However, Rubisco can fix carbon dioxide AND oxygen (carboxylation + oxygenation)
When concentration of carbon dioxide decreases + oxygen con increases, Rubisco is encouraged to fix oxygen instead (PHOTORESPIRATION) which does not produce sugars = less efficient use of ATP and no energy produced
(decreased co2 concentration increases affinity of rubisco for oxygen)
High temperatures also increases affinity of Rubisco to bind to oxygen
C4 SYSTEM
KRANZ ANATOMY = bundle sheath cells form a ring (thick with lots of chloroplasts) around vascular bundle tissue and mesophyll cells form an outer ring around the bundle sheath cells (wreath anatomy)
(high ratio of bundle sheath cells to mesophyll cells as the importance of these cells are required in order for Rubisco to fix carbon dioxide instead)
Requirement for C4: Plant structure must have two different compartments but close enough for metabolic exchange; gases (from outside) must reach PEP carboxylase first before Rubisco
In C4 plants, they have divided themselves into two different cell types (due to different gene expression as theres different function and position of plastids (chloroplasts)
METHOD:
- Carbon dioxide from outside is converted into bicarbonate (HCO3-) by CARBONIC ANHYDRASE (CA)
- Phosphoenolpyruvate Carboxylase (PEP carboxylase) is specific to bicarbonate where a carbon atom is fixed onto PHOSPHOENOLPYRUVATE forming a C4 molecule (oxaloacetate–>malate)
- C4 acids (oxaloacetates or derivatives) get transported into bundle sheath cells to get decarboxylased (releases carbon dioxide which gets actioned by Rubisco)
- C3 molecule (pyruvate; leftover) gets transported back into mesophyll cell to get carboxylated into C4 through PEP carboxylase (using ATP it is transformed into PEP)
C4 PLANTS
All the enzymes present in C3 plants are the same for C4 plants = easy for plants to acquire capability for C4 system
As all the required enzymes in C3 plants are present, we can genetically engineer features of C4 photosynthesis into C3 crop plants (e.g. rice, soybean)
The physiology of C4 plants are developmentally and environmentally controlled:
- The base of leaf (towards petiole + stem) is non-photosynthetic sink tissue and tip of leaf is C4 photosynthetic
- Plants with leaves underwater + in air (sedges) have different physiology, underwater leaves = C3 and leaves in air = C4
C4 plants = economically important (food staples, e.g. corn, sugar cane)
Importance/Advantage of C4
C4 system has the purpose to reduce photorespiration
Photorespiration = when rubisco binds to oxygen instead of carbon dioxide, wasting energy and decreasing sugar synthesis
Photorespiration increases at high temperatures as Rubisco selectivity decreases and solubility of carbon dioxide decrease (+ at high temperatures, stoma closes to prevent water loss = increased oxygen conc)
In C4 plants, without photorespiration, photosynthesis continues to increase with temperature as compared to C3 plants (but if photorespiration was supressed in C3 plants, they will have same growth rate)
C4 plants are most frequent in hot conditions (increases biomass accumulation in dry, sunny, hot regions)
C4 plants have the advantage with high temperatures as they are not carbon-limited, they can take advantage of high-light intensities
CAM System
Crassulacean Acid Metabolism
Night and day mechanism (but still consists of two different processes of carboxylation at different times)
NIGHT:
- PEP carboxylase fixes bicarbonate into C4 acids which is stored in vacuoles (occurs when stroma is open, allowing CO2 to come in)
- pH decreases due to accumulated carbon dioxide + acids
- Organic acids accumulate during the night and are metabolised during the day
DAY:
-Stored C4 acids gets decarboxylased into carbon dioxide by rubisco and C3 molecule follows cycle
Economic importance: vanilla, pineapple, aloe vera
Facultative CAM properties
Some plants can change their mechanisms depending on water availability
With low water, plants can transition to CAM system to reduce water loss (opening stomata at night)
When water availability increases, plant switches back to C3 system
CAM plants are often associated with low intercellular air spaces and air/mesophyll interfaces = often show succulence (large mesophyll cells with large vacuoles)
Strong ‘CAM plants’ require reduced intercellular air spaces and reduced exposure of mesophyll cells to reduce carbon dioxide loss
CAM vs C4
CAM: high temperatures, low water
C4: high temperatures, lots of water
Plant evolution of C4 and CAM plants
C4 phylogeny:
34 dicot lineages (~1700 species)
27 monocot lineages (~6000 species)
no C4 gymnosperms, byrophytes, or lower vascular plants
CAM:
6% of angiosperms are CAM plants (more widespread than C4 plants)
-CAM plants have arised long before C4 plants but diversity of C4 plants are increasing now due to alterations in carbon dioxide atmospshere
Transgenic Manipulations
Transgenic manipulations = genetic engineering
This was used to do research on modifying Rubisco used in carbon dioxide fixing
- Engineering CAM systems into plants to improve water-use efficiency
- Strategies to improve C4 photosynthesis (changing 1 gene to produce more efficient enzymes)
C4 RICE PROJECT:
Engineering C4 into rice crops to improve yield, water-use and nitrogen use
-incorporated changing the biochemistry of plant and plant anatomy
-able to create a line of 5 enzymes in the span of 6 years
-kranz anatomy was not able to be implemented but it did not matter (presence of required enzymes)
Pathogens and Diseases
Pathogen - disease causing microorganism
Disease - condition where normal function/structure of body part is damaged or impaired
(immune systems are evolutionary ancient, where they have evolved over time to be extremely complex nowadays)
All immune responses have 3 broad phases:
Recognition phase = organism must discriminate between self and non-self
Activation phase = mobilisation of cells and molecules to fight invader
Effector phase = Mobilized cells and molecules destroy invader
(mechanisms to accomplish this outcome ranges within phyla)
Components of mammalian immune system
Non specific innate immune response (I)
- first line of defense against pathogens
- lacks immunological memory
Specific adaptive immune response (A)
- resistance towards pathogen/agent
- has ‘memory’; increases effectiveness towards foreign agent due to repeated exposure
Other organisms have similar cells + functions
e.g. ‘amoebocytes’ are phagocytes in horseshoe crabs and other arthropods
Recognising pathogens
All immune responses begin with identifying foreign agent through specialised receptors present in cell
PRR (PATTERN RECOGNITION RECEPTORS):
There are 4 types:
CLR - c-type leptin receptors (transmembrane receptors; fungal and bacterial glycans (sugars)
NLR - nod like receptors (cytoplasmic receptor; different subfamilies recognise different foreign molecules from bacteria, viruses, fungi, parasites)
RLR - retanoic-acid-inducible gene 1-like receptor (cytoplasmic sensors of viral RNA; triggers antiviral responses)
TLR - toll like receptors (transmembrane in plasma membrane or endosome receptors; different TLRs recognise different molecules)
TLR Receptors
Found in invertebrates and vertebrates (demonstrating evolutionary ancient trait)
Different TLRs recognise different PAMPs (mammals have at least 10 TLRs)
PAMPs = pathogen associated molecular patterns
-can also be MAMPs in the wrong area
-can be MAMPs + DAMPs
examples:
TLR3 = found in endolysosomal system that detects double-stranded RNA (viruses)
TLR4 = found in plasma membrane for bacterial lipopolysaccharide; viral coat proteins (bacteria, virus)
TLR 5 = detects bacterial flagellin in plasma membrane
TLR 9 = endolysosomal system detecting unmethylated CpG DNA (bacteria, virus, protozoa)
(lots of ways for immune system to detect as arge range increases change of survival + decreases pathogen survival)
MAMPs = Microbial Associated Molecular Patterns
-carbohydates, proteins, nucleic acid molecules expressed by bacteria, viruses and parasites
DAMPs = damage associated molecular patterns
- signals of damage to an endogenous (internal cell) by a pathogen
- membrane damage, molecules released due to stress, dead or dying cells, signals of tissue damage
Activation of immune system
PRRs sensing PAMPs leads to activation (all begins with non-specific innate response)
-Secretion of defensins or other antimicrobial peptides
Defensins = type of antimicrobial peptide (ancient form of defense = found in majority of animals)
Defensins are small, positively charged polypeptide (<100AA) (bacterias have the same = bacteriocins are the equivalent)
Defensins disrupt the structural integrity of pathogen membranes + some viral envelopes (defensins are positively charged whilst phospholipid tails are negatively charged = draws defensins inside; protected agents inside will leak out)
- Production of pro-inflammatory cytokines
- Activation of complement system
-Phagocytosis
Process where pathogens are disposed where phagocytic vacuoles (vesicle formed = phagosome) engulfs cell
(phagocytosis can activate production of pro-inflammatory cytokines; recruits more immune cells to site of injury/threat)
Phagocytosis can also activate specific adaptive immune response (linkage between innate and adaptive system)
Phagocytes present the antigen on pathogen on the membrane to present to T helper cells (PAMPs (antigens) are digested and presented on cell surface where phagocyte becomes an ACTIVATED DENDRITIC CELL)
Activated dendritic cells travel throughout lymph node where helper T cells have different antibody receptors that can bind to antigen (on macrophage)
When a match is found, T cells travel to the site of injury/threat and activate B cells (proliferation and differentiation of t and b cells occur)
Adaptive Response
Antigen = a molecule that can induce adaptive immune response or that can bind to an antibody or T cell receptor Antibody = proteins that bind to a specific antigen, can be expressed on cell surface or secreted
B cells:
-B cells mature in the bone marrow (type of lymphocyte)
-B cells either become Memory B cells (long lived B cells that can produce specific antibodies to recently introduced antigen) or Antibody secreting plasma cells (produces antibodies that tightly binds to target pathogens = inactivating it or marks it for destruction)
Memory B cells allows secondary response to antigen faster + more efficient
T cells:
-Matures in the thymus
-Activated by phagocytic cells where they specialise into Helper cells or Cytotoxic cells (effector cells)
Cytotoxic cells (Tc) = kills infected cells
Helper T cells = amplifies response by releasing cytokines to recruit further Tc cells + phagocytes (clean up or kill pathogen)
Diversity of T and B cell receptors
T and B cell clones travel throughout body but each clone recognises a different antigen (large variety but small amount)
Diversity of these cells are due to V(D)J recombination
- the genome of T and B cells undergoes random rearrangement of a set of regions known as V, D and J (all are genes responsible for coding antibodies)
- a combination of these genes forms a functional exon (when individual, they are not functional)
- different combinations of VD and J = different antigen binding sites = different antigens recognised
Comparisons between animal and plant immunity
Animal:
- Basal innate immunity (always present)
- Innate complement system (aids the activities of both adaptive + innate immune response by marking pathogens)
- Adaptive immune response (we have antibodies + specialised cells)
Plants:
-no circulating antibodies or cells (each plant cell must be able to defend itself)
-structural barriers (cell walls, cuticles)
-Basal innate immunity = pathogen triggered immunity (PTI) (similar to PRR)
-Effector triggered immunity (ETI) = their specific response (PTI (pathogen identified) –> pathogen effectors can suppress defense response (effector triggered susceptibility) which stops PTI)
ETI can recognise resistance gene and is activated (specific to antigen but has no memory)
-adaptive systemic signals from infection sites (systemic acquired resistance) = signals to other cells of danger/threat allowing adjacent cells to prepare for defense
-can secrete toxic molecules, allowing cell death
Bacterial adaptive defenses
CRISPR system = clustered regularly interspaced short palindromic repeats
If bacteria is infected by a phage, the secreted material is recorded in CRISPR arrays (nucleic acids in array is identical to phage)
As the sequence of phage is in the bacteria, it can be expressed to make CRISPR RNA (transcription of RNA)
Transcription forms CAS PROTEIN = marks targets for destruction by bacterial cellular machinery (DNA in RNA matches phage; how CAS protein can differentiate the phage from bacterial cells)
Vaccinations
Dead, attenuated (weakened) pathogen material injected to stimulate adaptive innate response (establishing immunity memory)
Vaccinations only work for animals with adaptive immune response
Top 10 microbes of Irwin’s List
- Irish potato blight (oomycete, protist)
- Malaria (apicomplexa, protist)
- Cholera (bacterium)
- Bubonic plague (bacterium)
- Syphillis (bacterium)
- Tuberculosis (bacterium)
- Smallpox (virus)
- Yellow fever (virus)
- AIDS (virus)
- Influenza (virus)
Types of Microbes that cause disease (Virus)
Viruses = infectious agents
- not cellular, cannot self-replicate
- needs a host to make copies of themself
- compromised of a genome (DNA or RNA), capsid (protein) and sometimes an external membrane (capsule, lipid, envelope)
- no ribosomes, organelles, energy metabolism
- very small (~1 nm)
Despite successful eradication of some viruses (e.g. smallpox), the re-emergence of viral diseases are a regular occurence (e.g. SARS, HIV, ebola, MERS, Zika)
-viruses are difficult to treat as they hijack host’s cellular machinery for replication (stopping cellular mechanisms may hurt host’s cells)
