Description of Eurystomatella sinica n. gen., n. sp., with establishment of a new family Eurystomatellidae n. fam. (Protista, Ciliophora, Scuticociliatia) and analyses of its phylogeny inferred from sequences of the small-subunit rRNA gene
PISCINOODINIUM, A FISH-ECTOPARASITIC DINOFLAGELLATE, IS A MEMBER OF THE CLASS DINOPHYCEAE, SUBCLASS GYMNODINIPHYCIDAE: CONVERGENT EVOLUTION WITH AMYLOODINIUM
"These molecular and morphological data suggest that evolution of this mode of fish ectoparasitism occurred independently in 2 distantly related groups of dinoflagellates, and they further suggest that the taxonomic status of parasites grouped as members of Piscinoodinium requires major revision."
Here's where I'm at on the list, so far - everything on the list above it looks like it could be involved in disease. Human disease could be related to what the bats, frogs, bees, and koalas, and why not include the fish? I'm thinking what's in the ocean might be the main source for all...
"The inedible fungus Daldinia concentrica is known by several common names, including King Alfred's Cake, cramp balls, and coal fungus.
D. concentrica contains several unique compounds, including a metabolite called concentricol, which is oxidized squalene. Many types of insects and other small animals make their home inside this species of fungus."
**So, there is a coal-like fungus found in nature that inside can live a variety of 'critters'... oxidized squalene... hmmm?
""There has been a lot of research looking at the climate effects of man-made aerosols," Christopher said. "Particles from smoke and burning fossil fuels are tiny, sub-micron size. These tiny particles cool the atmosphere because they reflect sunlight back into space before it has a chance to heat the air. That means less solar energy is available at the surface to heat the planet."
Because they are so small, pollution aerosols don't have a significant effect on heat energy. That's why they usually have a net cooling effect on the atmosphere."
"ScienceDaily (Dec. 29, 2006) — More than half of the dust needed for fertilizing the Brazilian rainforest is supplied by a valley in northern Chad, according to an international research team headed by Dr. Ilan Koren of the Institute's Environmental Sciences and Energy Research Department."
Arctic Glacial Dust May Affect Climate and Health in North America and Europe
"ScienceDaily (Feb. 20, 2010) — Residents of the southern United States and the Caribbean have seen it many times during the summer months -- a whitish haze in the sky that seems to hang around for days. The resulting thin film of dust on their homes and cars actually is soil from the deserts of Africa, blown across the Atlantic Ocean."
"Australian scientists have discovered an ancient protein which is providing new clues to understanding some of the earliest steps in the evolution of life.
The Omp85 family of proteins, recently discovered by scientists at the University of Melbourne, is now believed to have played a crucial role in creating the first eukaryotes, complex cells that eventually gave rise to organisms ranging from single-celled yeasts and algae to complex creatures like humans.
Scientists believe that genes from the bacteria somehow managed to make their way to the nucleus of the cell in which they lived, and the first eukaryotic cells were born.
The bacteria, which had previously been parasites that lived inside the cell, had effectively transformed into the organelles we now know as mitochondria. They were controlled by the host cell and used as power houses.
But housing a cell within a cell created new problems. And how the host cell could force the growth and division of the enslaved bacteria is a question that has continued to perplex scientists.
Lithgow says the trick early on in evolution was for the host cell to deliver some of its own protein molecules back into the bacterium to force its growth and division and form new bacteria, or, mitochondria.
That way the host cell has enough power, and has enough mitochondria for every time the cell needs to divide. But for a long time weve been in the dark about how proteins and other molecules could be delivered across the membranes that encase the bacterium/mitochondria.
Now, he believes they may have found the answer.
... recently discovered that the Omp85 proteins exist in all living cells from humans to animals to plants.
During evolution, the early host cell took control and used Omp85 to drive protein and lipid transport back into the bacteria as they became mitochondria.
He says, The bacteria that cause meningitis stimulate human cells to die by injecting pore proteins from their own outer membranes into the human cells. Once injected, the bacterial pore protein probably seeks its cousin, Omp85, to be inserted into the mitochondrial membranes. We suspect it forms large pores in the mitochondria, leaching their contents and eventually causing the infected cells to die.
Understanding how Omp85 transports protein and lipid molecules, including the bacterial pore proteins, into membranes will provide the knowledge we need to design therapies to block bacterial infection."
"The modification process often tries to lower the amount of oxygen (O2), moving it from 20% to 0%, In order to slow down the growth of aerobic organisms and the speed of oxidation reactions. The removed oxygen can be replaced with nitrogen (N2), commonly acknowledged as an inert gas, or carbon dioxide (CO2), which can lower the pH or inhibit the growth of bacteria. Carbon monoxide can be used for keeping the red color of meat."
"Senescence or biological aging is the change in the biology of an organism as it ages after its maturity. There are a number of theories as to why senescence occurs, including ones that claim it is programmed by gene expression changes and that it is the accumulative damage of biological processes.
Cellular senescence is the phenomenon by which normal diploid cells lose the ability to divide, normally after about 50 cell divisions in vitro. Some cells become senescent after fewer replications cycles as a result of DNA double strand breaks, toxins, etc. This phenomenon is also known as "replicative senescence", the "Hayflick phenomenon", or the Hayflick limit...
In response to DNA damage (including shortened telomeres), cells either age or self-destruct (apoptosis, programmed cell death) if the damage cannot be repaired. In this 'cellular suicide', the death of one cell, or more, may benefit the organism as a whole. For example, in plants the death of the water-conducting xylem cells (tracheids and vessel elements) allows the cells to function more efficiently and so deliver water to the upper parts of a plant.
Aging of the whole organism
Organismal senescence is the aging of whole organisms. In general, aging is characterized by the declining ability to respond to stress, increased homeostatic imbalance, and increased risk of aging-associated diseases.
Theories of aging
However, senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species because it prevents the onset of cancer. In a few simple species, such as Hydra, senescence is negligible and cannot be detected. All such species have no "post-mitotic" cells; they reduce the effect of damaging free radicals by cell division and dilution. Such species are not immortal, however, as they will eventually fall prey to trauma or disease. Moreover, average lifespans can vary greatly within and between species. This suggests that both genetic and environmental factors contribute to aging.
Stochastic theories blame environmental impacts on living organisms that induce cumulative damage at various levels as the cause of aging, examples of which ranging from damage to DNA, damage to tissues and cells by oxygen radicals (widely known as free radicals countered by the even more well-known antioxidants), and cross-linking.
A gene can be expressed at various life-stages.
It is thought that strategies that result in a higher reproductive rate at a young age, but shorter overall lifespan, result in a higher lifetime reproductive success and are therefore favoured by natural selection. In essence, aging is, therefore, the result of investing resources in reproduction, rather than maintenance of the body (the "Disposable Soma" theory), in light of the fact that accidents, predation, and disease will eventually kill the organism no matter how much energy is devoted to repair of the body.
Therefore, late-acting deleterious mutations could accumulate in populations over evolutionary time through genetic drift. This principle has been demonstrated experimentally. And it is these later-acting deleterious mutations that are believed to cause—even allow—age-related mortality.
Peter Medawar formalised this observation in his mutation accumulation theory of aging. "The force of natural selection weakens with increasing age—even in a theoretically immortal population, provided only that it is exposed to real hazards of mortality. If a genetic disaster… happens late enough in individual life, its consequences may be completely unimportant". The 'real hazards of mortality' are, in typical circumstances, predation, disease, and accidents. So, even an immortal population, whose fertility does not decline with time, will have fewer individuals alive in older age groups. This is called 'extrinsic mortality'. Young cohorts, not depleted in numbers yet by extrinsic mortality, contribute far more to the next generation than the few remaining older cohorts, so the force of selection against late-acting deleterious mutations, which affect only these few older individuals, is very weak. The mutations may not be selected against, therefore, and may spread over evolutionary time into the population.
The major testable prediction made by this model is that species that have high extrinsic mortality in nature will age more quickly and have shorter intrinsic lifespans.
Another evolutionary theory of aging was proposed by George C. Williams and involves antagonistic pleiotropy. A single gene may affect multiple traits. Some traits that increase fitness early in life may also have negative effects later in life. But, because many more individuals are alive at young ages than at old ages, even small positive effects early can be strongly selected for, and large negative effects later may be very weakly selected against. Williams suggested the following example: Perhaps a gene codes for calcium deposition in bones, which promotes juvenile survival and will therefore be favored by natural selection; however, this same gene promotes calcium deposition in the arteries, causing negative effects in old age. Therefore, negative effects in old age may reflect the result of natural selection for pleiotropic genes that are beneficial early in life. In this case, fitness is relatively high when Fisher's reproductive value is high and relatively low when Fisher's reproductive value is low.
A number of genetic components of aging have been identified using model organisms, ranging from the simple budding yeast Saccharomyces cerevisiae to worms such as Caenorhabditis elegans and fruit flies (Drosophila melanogaster). Study of these organisms has revealed the presence of at least two conserved aging pathways.
One of these pathways involves the gene Sir2, a NAD+-dependent histone deacetylase. In yeast, Sir2 is required for genomic silencing at three loci: The yeast mating loci, the telomeres and the ribosomal DNA (rDNA). In some species of yeast, replicative aging may be partially caused by homologous recombination between rDNA repeats; excision of rDNA repeats results in the formation of extrachromosomal rDNA circles (ERCs). These ERCs replicate and preferentially segregate to the mother cell during cell division, and are believed to result in cellular senescence by titrating away (competing for) essential nuclear factors. ERCs have not been observed in other species (nor even all strains of the same yeast species) of yeast (which also display replicative senescence), and ERCs are not believed to contribute to aging in higher organisms such as humans (they have not been shown to accumulate in mammals in a similar manner to yeast). Extrachromosomal circular DNA (eccDNA) has been found in worms, flies, and humans. The origin and role of eccDNA in aging, if any, is unknown.
Despite the lack of a connection between circular DNA and aging in higher organisms, extra copies of Sir2 are capable of extending the lifespan of both worms and flies (though, in flies, this finding has not been replicated by other investigators, and the activator of Sir2 resveratrol does not reproducibly increase lifespan in either species). Whether the Sir2 homologues in higher organisms have any role in lifespan is unclear, but the human SIRT1 protein has been demonstrated to deacetylate p53, Ku70, and the forkhead family of transcription factors. SIRT1 can also regulate acetylates such as CBP/p300, and has been shown to deacetylate specific histone residues.
RAS1 and RAS2 also affect aging in yeast and have a human homologue. RAS2 overexpression has been shown to extend lifespan in yeast.
Other genes regulate aging in yeast by increasing the resistance to oxidative stress. Superoxide dismutase, a protein that protects against the effects of mitochondrial free radicals, can extend yeast lifespan in stationary phase when overexpressed.
In higher organisms, aging is likely to be regulated in part through the insulin/IGF-1 pathway. Mutations that affect insulin-like signaling in worms, flies, and the growth hormone/IGF1 axis in mice are associated with extended lifespan. In yeast, Sir2 activity is regulated by the nicotinamidase PNC1. PNC1 is transcriptionally upregulated under stressful conditions such as caloric restriction, heat shock, and osmotic shock. By converting nicotinamide to niacin, nicotinamide is removed, inhibiting the activity of Sir2. A nicotinamidase found in humans, known as PBEF, may serve a similar function, and a secreted form of PBEF known as visfatin may help to regulate serum insulin levels."
it is widely believed that cellular senescence evolved as a way to prevent the onset and spread of cancer. Somatic cells that have divided many times will have accumulated DNA mutations and would therefore be in danger of becoming cancerous if cell division continued.
Cancer cells are usually immortal.
Lately, the role of telomeres in cellular senescence has aroused general interest, especially with a view to the possible genetically adverse effects of cloning. The successive shortening of the chromosomal telomeres with each cell cycle is also believed to limit the number of divisions of the cell, thus contributing to aging. There have, on the other hand, also been reports that cloning could alter the shortening of telomeres. Some cells do not age and are, therefore, described as being "biologically immortal". It is theorized by some that when it is discovered exactly what allows these cells, whether it be the result of telomere lengthening or not, to divide without limit that it will be possible to genetically alter other cells to have the same capability. It is further theorized that it will eventually be possible to genetically engineer all cells in the human body to have this capability by employing gene therapy and, therefore, stop or reverse aging, effectively making the entire organism potentially immortal.
In about 85% of tumors, this evasion of cellular senescence is the result of up-activation of their telomerase genes. This simple observation suggests that reactivation of telomerase in healthy individuals could greatly increase their cancer risk.
Whether cell senescence plays any role in organismal aging is at present unknown, and is an active area of investigation. Mouse mutants lacking telomerase do not immediately show accelerated aging.
One of the earliest aging theories was the Rate of Living Hypothesis described by Raymond Pearl in 1928(based on earlier work by Max Rubner), which states that fast basal metabolic rate corresponds to short maximum life span.
While there may be some validity to the idea that for various types of specific damage detailed below that are by-products of metabolism, all other things being equal, a fast metabolism may reduce lifespan, in general this theory does not adequately explain the differences in lifespan either within, or between, species. Calorically-restricted animals process as much, or more, calories per gram of body mass, as their ad libitum fed counterparts, yet exhibit substantially longer lifespans.
With respect to specific types of chemical damage caused by metabolism, it is suggested that damage to long-lived biopolymers, such as structural proteins or DNA, caused by ubiquitous chemical agents in the body such as oxygen and sugars, are in part responsible for aging. The damage can include breakage of biopolymer chains, cross-linking of biopolymers, or chemical attachment of unnatural substituents (haptens) to biopolymers.
Under normal aerobic conditions, approximately 4% of the oxygen metabolized by mitochondria is converted to superoxide ion, which can subsequently be converted to hydrogen peroxide, hydroxyl radical and eventually other reactive species including other peroxides and singlet oxygen, which can, in turn, generate free radicals capable of damaging structural proteins and DNA. Certain metal ions found in the body, such as copper and iron, may participate in the process. (In Wilson's disease, a hereditary defect that causes the body to retain copper, some of the symptoms resemble accelerated senescence.) These processes are termed oxidative damage and are linked to the benefits of nutritionally derived polyphenol antioxidants.
Sugars such as glucose and fructose can react with certain amino acids such as lysine and arginine and certain DNA bases such as guanine to produce sugar adducts, in a process called glycation. These adducts can further rearrange to form reactive species, which can then cross-link the structural proteins or DNA to similar biopolymers or other biomolecules such as non-structural proteins. People with diabetes, who have elevated blood sugar, develop senescence-associated disorders much earlier than the general population, but can delay such disorders by rigorous control of their blood sugar levels. There is evidence that sugar damage is linked to oxidant damage in a process termed glycoxidation.
Free radicals can damage proteins, lipids or DNA. Glycation mainly damages proteins. Damaged proteins and lipids accumulate in lysosomes as lipofuscin. Chemical damage to structural proteins can lead to loss of function; for example, damage to collagen of blood vessel walls can lead to vessel-wall stiffness and, thus, hypertension, and vessel wall thickening and reactive tissue formation (atherosclerosis); similar processes in the kidney can lead to renal failure. Damage to enzymes reduces cellular functionality. Lipid peroxidation of the inner mitochondrial membrane reduces the electric potential and the ability to generate energy. It is probably no accident that nearly all of the so-called "accelerated aging diseases" are due to defective DNA repair enzymes.
It is believed that the impact of alcohol on aging can be partly explained by alcohol's activation of the HPA axis, which stimulates glucocorticoid secretion, long-term exposure to which produces symptoms of aging.
Main article: Reliability theory of aging and longevity
Reliability theory suggests that biological systems start their adult life with a high load of initial damage. Reliability theory is a general theory about systems failure. It allows researchers to predict the age-related failure kinetics for a system of given architecture (reliability structure) and given reliability of its components. Reliability theory predicts that even those systems that composed entirely of non-aging elements (with a constant failure rate) will nevertheless deteriorate (fail more often) with age, if these systems are redundant in irreplaceable elements. Aging, therefore, is a direct consequence of systems.
Recently, a kind of early senescence has been alleged to be a possible unintended outcome of early cloning experiments. The issue was raised in the case of Dolly the sheep, following her death from a contagious lung disease. The claim that Dolly's early death involved premature senescence has been vigorously contested, and Dolly's creator, Dr. Ian Wilmut has expressed the view that her illness and death were probably unrelated to the fact that she was a clone.
A set of rare hereditary (genetic) disorders, each called progeria, has been known for some time. Sufferers exhibit symptoms resembling accelerated aging, including wrinkled skin. The cause of Hutchinson–Gilford progeria syndrome was reported in the journal Nature in May 2003. This report suggests that DNA damage, not oxidative stress, is the cause of this form of accelerated aging."
"Classical theories1, 2 for the evolution of senescence predict that organisms that experience low mortality rates attributable to external factors, such as disease or predation, will evolve a later onset of senescence.
We report here that these same populations do not have an earlier onset of senescence with respect to either mortality or reproduction but do with respect to swimming performance, which assesses neuromuscular function.
This mosaic pattern of senescence challenges the generality of the association between decreased extrinsic mortality and delayed senescence and invites consideration of more derived theories for the evolution of senescence."
** Well, other than the fact that we won't get our pension plans, they get back our homes, they get a part of our estate through taxing, sometimes we donate our life's work to their charities or universities, and can b.s. manipulate the younger generation easier... this abstract says that "to swimming performance, which assesses neuromuscular function" is the reason the guppies live longer lives. Yes, take away physical education in the schools, feed the young a diet deficient so that they have no chance of a long life. And, most of all we don't want any elders around to guide the young.
Their science is fowled with unknowns, we're going to answer some of their questions, looks like we're human guinea pigs in an evolution of senescence experiment?
"This requires that death occur from injury or disease rather than deterioration, i.e., the absence of cellular senescence.
"Biologists have chosen the word immortal to designate cells that are not limited by the Hayflick limit (where cells no longer divide because of DNA damage or shortened telomeres). Prior to Leonard Hayflick, Alexis Carrel hypothesized that all normal somatic cells are immortal.
The term immortalization was first applied to cancer cells that expressed the telomere-lengthening enzyme telomerase, and thereby avoided apoptosis (cell death caused by intracellular mechanisms). Among the most commonly used cell lines are HeLa and Jurkat, both of which are immortalized cancer cell lines. Normal stem cells and germ cells can also be said to be immortal (when humans refer to the cell line).
Immortal cell lines of cancer cells can be created by induction of oncogenes or loss of tumor suppressor genes. One way to induce immortality is through viral-mediated induction of the large T-antigen, commonly introduced through simian virus 40 (SV-40).
Tardigrades, otherwise known as "water bears" are highly resilient microscopic animals. They have indefinite senescence; moreover, unlike bacteria, they are incredibly difficult to destroy. Capable of surviving extremes such as heat, radiation, drought, and even the vacuum of space by going into suspended animation, where their metabolism slows to near zero and they simply wait out the harsh conditions until the environment is more favorable. The Russian Space Administration is planning a mission to launch water bears at Phobos to study the scientific theory of panspermia."
"Tardigrades (commonly known as water bears or moss piglets) form the phylum Tardigrada, part of the superphylum Ecdysozoa. They are microscopic, water-dwelling, segmented animals with eight legs."
Turritopsis nutricula is a small (5 millimeters (0.2 in)) species of jellyfish which uses transdifferentiation to replenish cells after sexual reproduction. This cycle can repeat indefinitely, potentially rendering it biologically immortal. It originated from the Caribbean sea, but has now spread around the world."
Research has shown that selective breeding can dramatically extend fruit fly lifespans. The technique involved repeatedly cultivating eggs from fruit flies that maintained enough of their physiological function to reproduce in old age. This delayed-reproduction lineage lives up to five times longer than average."
"In a few simple species, such as Hydra, senescence is negligible and cannot be detected. All such species have no "post-mitotic" cells; they reduce the effect of damaging free radicals by cell division and dilution. Such species are not immortal, however, as they will eventually fall prey to trauma or disease."
It's octopus-like, or 'stellar-shaped' as described in our case study and what's in the trees, isn't that interesting?:
"Stochastic theories blame environmental impacts on living organisms that induce cumulative damage at various levels as the cause of aging, examples of which ranging from damage to DNA, damage to tissues and cells by oxygen radicals (widely known as free radicals countered by the even more well-known antioxidants), and cross-linking."
**In certain lesions - polymerization crosslinking and crosslinking malfunction of our DNA:
In the biological sciences, crosslinking typically refers to a more specific reaction used to probe molecular interactions. For example, proteins (a type of natural polymer) can be cross-linked together using small-molecule crosslinkers. In biological tissue, crosslinks can be induced as disulfide bonds between collagen fibrils. Compromised collagen in the cornea, a condition known as keratoconus, can be treated with clinical crosslinking.
Uses for crosslinked polymers
Synthetically crosslinked polymers have many uses, including those in the biological sciences, such as applications in forming polyacrylamide gels for gel electrophoresis.
Crosslinks in DNA occur when various exogenous or endogenous agents react with two different positions in the DNA. This can either occur in the same strand (intrastrand crosslink) or in the opposite strands of the DNA (interstrand crosslink). Crosslinks also occur between DNA and protein. DNA replication is blocked by crosslinks, which causes replication arrest and cell death if the crosslink is not repaired.
The RAD51 family plays a role in repair.
Agents that Crosslink DNA
I. Exogenous Cross Linking Agents Alkylating agents such as 1, 3-bis(2-chloroethyl)-1-nitrosourea (BCNU, Carmustine)) and Nitrogen mustard which are used in chemotherapy can cross link with DNA at N7 position of guanine on the opposite strands forming interstrand crosslink. Cisplatin (cis-diamminedichloroplatinum(II)) and its derivative forms DNA cross links as monoadduct, interstrand crosslink, intrastrand crosslink or DNA protein crosslink. Mostly it acts on the adjacent N-7 guanine forming 1, 2 intrastrand crosslink.
II. Endogenous Cross Linking Agents
Nitrous acid formed in the stomach dietary source nitrites. It induces formation of interstrand DNA crosslink at aminogroup of exocyclic N2 of guanine at the CG sequences. Reactive chemicals such as malondialdehyde which are formed endogenously as the product of lipid peroxidation. They create etheno adducts formed by aldehyde which undergo rearrangements to form crosslinks on opposite strands.
Psoralens are natural compounds (furocoumarins) present in plants. These compounds get activated in the presence of UV - A. They form covalent adducts with pyrimidines. Covalent adducts are formed by linking 3, 4 (pyrone) or 4', 5’ (furan) edge of psoralen to 5, 6 double bond of thymine. Psoralens can form two types of monoadducts and one diadduct (an interstrand crosslink) reacting with thymine. The crosslinking reaction by Psoralens targets TA sequences intercalating in DNA and linking one base of the DNA with the one below it. Psoralen adducts cause replication arrest and is used in the treatment of psoriasis and vitiligo. Aldehydes such as acrolein and crotonaldehyde found in tobacco smoke or automotive exhaust can form DNA interstrand crosslinks in DNA. Guanine adducts of DNA can also react with protein. A Schiff base formation between protein and aldehyde causes this DNA protein interstrand link
Formaldehyde (HCHO) induces protein-DNA and protein-protein crosslinks, and is a common reagent of choice for molecular biology experiments. These crosslinks may be reversed by incubation at 70°C."
In humans, RAD51 is a 339-amino acid protein that plays a major role in homologous recombination of DNA during double strand break repair.
The structural basis for Rad51 filament formation and its functional mechanism still remain poorly understood. However, recent studies using fluorescent labeled Rad51 has indicated that Rad51 fragments elongate via multiple nucleation events followed by growth, with the total fragment terminating when it reaches about 2 μm in length. Disassociation of Rad51 from dsDNA, however, is slow and incomplete, suggesting that there is a separate mechanism that accomplishes this.
This protein is also found to interact with BRCA1 and BRCA2, which may be important for the cellular response to DNA damage.
BRCA2 is shown to regulate both the intracellular localization and DNA-binding ability of this protein. Loss of these controls following BRCA2 inactivation may be a key event leading to genomic instability and tumorigenesis.
The Rad51 gene is located on chromosome 15 and several alterations of the gene have been associated with an increased risk of developing breast cancer. The breast cancer susceptibility protein BRCA2 controls the function of Rad51 in the pathway for DNA repair by homologous recombination. Increased RAD51 expression levels have been identified in metastatic canine mammary carcinoma, indicating that genomic instability plays an important role in the carcinogenesis of this tumor type.
RAD51 has been shown to interact with BRE, RAD54B, Ataxia telangiectasia mutated, BRCC3, BARD1, BRCA2, UBE2I, Abl gene, BRCA1, ATRX, RAD52, DMC1, P53 and Bloom syndrome protein."
"When a cell prepares to divide to form two cells, the chromosomes are duplicated so that each new cell will get a complete set of chromosomes. The duplication process is called DNA replication. Errors made during DNA replication can lead to mutations. The BLM protein is important in maintaining the stability of the DNA during the replication process. The mutations in the BLM gene associated with Bloom syndrome inactivate the BLM protein's DNA helicase activity or nullify protein expression (the protein is not made)."
Main article: Polymerase chain reaction Researchers commonly replicate DNA in vitro using the polymerase chain reaction (PCR). PCR uses a pair of primers to span a target region in template DNA, and then polymerizes partner strands in each direction from these primers using a thermostable DNA polymerase. Repeating this process through multiple cycles produces amplification of the targeted DNA region. At the start of each cycle, the mixture of template and primers is heated, separating the newly synthesized molecule and template. Then, as the mixture cools, both of these become templates for annealing of new primers, and the polymerase extends from these. As a result, the number of copies of the target region doubles each round, increasing exponentially."
"Other forms of genetic engineering include gene targeting and knocking out specific genes via engineered nucleases such as zinc finger nucleases or engineered homing endonucleases.
Genetic engineering techniques have been applied in numerous fields including research, biotechnology, and medicine. Medicines such as insulin and human growth hormone are now produced in bacteria, experimental mice such as the oncomouse and the knockout mouse are being used for research purposes and insect resistant and/or herbicide tolerant crops have been commercialized. Genetically engineered plants and animals capable of producing biotechnology drugs more cheaply than current methods (called pharming) are also being developed and in 2009 the FDA approved the sale of the pharmaceutical protein antithrombin produced in the milk of genetically engineered goats.
Genetic engineering alters the genetic makeup of an organism using techniques that introduce heritable material prepared outside the organism either directly into the host or into a cell that is then fused or hybridized with the host. This involves using recombinant nucleic acid (DNA or RNA) techniques to form new combinations of heritable genetic material followed by the incorporation of that material either indirectly through a vector system or directly through micro-injection, macro-injection and micro-encapsulation techniques.
Synthetic biology is an emerging discipline that takes genetic engineering a step further by introducing artificially synthesized genetic material from raw materials into an organism."
"Humans have altered the genomes of species for thousands of years through artificial selection and more recently mutagenesis. Genetic engineering as the direct manipulation of DNA by humans outside breeding and mutations has only existed since the 1970s.
Once isolated, the gene is inserted into a bacterial plasmid.
"Plasmids used in genetic engineering are called vectors. Plasmids serve as important tools in genetics and biotechnology labs, where they are commonly used to multiply (make many copies of) or express particular genes."
tash: Hi skizit, I have watched all your videos on youtube and cant thank you enough for all you have educated me on. I cry for you alot and a bit for me. I was wanting to send you photos of what is raining down everyday here in Australia in hope you can tell me
Dec 11, 2019 23:28:22 GMT -5
tash: not sure where to send them as hush mail and rocket mail bounced back
Dec 11, 2019 23:30:03 GMT -5