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Cells Module 3 short
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1ALL YOU REQUIRE FOR NATURAL SELECTION IS:
[blank_start]Variation[blank_end]: individuals in a population vary from one another
[blank_start]Inheritance[blank_end]: parents pass on their traits to their offspring genetically
[blank_start]Selection[blank_end]: some variants reproduce more than others
[blank_start]Time[blank_end]: successful variations accumulate over many generations
[blank_start]Natural[blank_end] selection: those with traits [blank_start]useful[blank_end] for [blank_start]survival[blank_end] are [blank_start]more[blank_end] likely to [blank_start]survive[blank_end] and be able to [blank_start]reproduce[blank_end]
[blank_start]Sexual[blank_end] selection: those with traits that make them [blank_start]appealing[blank_end] to the [blank_start]opposite sex[blank_end], and not necessarily [blank_start]useful[blank_end] for [blank_start]survival[blank_end], will [blank_start]reproduce more[blank_end] e.g. peacock tails.- AVariation
- BInheritance
- CSelection
- DTime
- ENatural
- Fuseful
- Gsurvival
- Hmore
- Isurvive
- Jreproduce
- KSexual
- Lappealing
- Mopposite sex
- Nuseful
- Osurvival
- Preproduce more
2Allan Wilson studied evolution using [blank_start]biological molecules[blank_end] (which also evolve over [blank_start]time[blank_end]). He showed that [blank_start]relationships[blank_end] between species could be [blank_start]reconstructed[blank_end] from [blank_start]changes[blank_end] in a [blank_start]molecule[blank_end], more [blank_start]change[blank_end] = more [blank_start]distance[blank_end]. Humans and chimps and [blank_start]99[blank_end]% similar, all [blank_start]humans[blank_end] descended from a [blank_start]single common female ancestor[blank_end] 60,000 years ago and humans and chimps separated about [blank_start]6[blank_end] million years ago. Evolution can explain [blank_start]Anatomy[blank_end], the origins of [blank_start]microbial[blank_end] resistance, our [blank_start]immune[blank_end] system and some [blank_start]human[blank_end] disease. Evolutionary medicine is becoming more important.
- Abiological molecules
- Btime
- Crelationships
- Dreconstructed
- Echanges
- Fmolecule
- Gchange
- Hdistance
- I99
- Jhumans
- Ksingle common female ancestor
- L6
- MAnatomy
- Nmicrobial
- Oimmune
- Phuman
3DNA replication - double helix, [blank_start]self-replicates[blank_end] within cells, can also be [blank_start]replicated[blank_end] in a [blank_start]test tube[blank_end], [blank_start]synthesises[blank_end] each strand [blank_start]individually[blank_end] so end up with [blank_start]two[blank_end] perfect [blank_start]copies[blank_end].
PCR (Polymerase Chain Reaction) - use flanking [blank_start]primers[blank_end] to [blank_start]synthesis[blank_end] many copies of the [blank_start]region of DNA[blank_end] that lies between, copying by [blank_start]synthesis[blank_end]
Recombinant DNA - [blank_start]DNA code[blank_end] is [blank_start]universal[blank_end] so whether it is s[blank_start]ynthetic[blank_end] or P[blank_start]CR[blank_end] or n[blank_start]atural[blank_end], you can put it anywhere, DNA can be [blank_start]copied[blank_end] and [blank_start]stuck[blank_end] together with all sorts of bits, turtle people
Chain Termination DNA Sequencing (Sanger) - works by [blank_start]synthesis[blank_end], making many [blank_start]labelled[blank_end] copies of the [blank_start]DNA[blank_end] and separating by [blank_start]size[blank_end]
Aligning sequences - sequences of DNA that [blank_start]overlap[blank_end] can be [blank_start]aligned[blank_end] using computers and assembled into [blank_start]longer fragments[blank_end]- Aself-replicates
- Breplicated
- Ctest tube
- Dsynthesises
- Eindividually
- Ftwo
- Gcopies
- Hprimers
- Isynthesise
- Jregion of DNA
- Ksynthesis
- Luniversal
- MDNA code
- Nynthetic
- OCR
- Patural
- Qcopied
- Rstuck
- Ssynthesis
- Tlabelled
- Usize
- VDNA
- Woverlap
- Xaligned
- Ylonger fragments
4The idea of DNA [blank_start]sequencing[blank_end] is that you [blank_start]synthesise[blank_end] a copy and [blank_start]label[blank_end] the strands that are added, can therefore identify the [blank_start]original sequence[blank_end].
Need:
1. target DNA: [blank_start]single[blank_end] template strand, always goes in [blank_start]one direction[blank_end] from [blank_start]5[blank_end]’ to [blank_start]3[blank_end]’
2. primer: a [blank_start]synthetic[blank_end] o[blank_start]ligonucleotide[blank_end] [blank_start]complementary[blank_end] to the [blank_start]known[blank_end] sequence, will [blank_start]bind[blank_end] and start [blank_start]copy[blank_end]
3. DNA polymerase: [blank_start]enzyme[blank_end] that cells use to [blank_start]copy[blank_end] DNA
4. nucleotides: dATP, dCTP, dTTP, dGTP, [blank_start]polymerase[blank_end] finds [blank_start]complementary nucleotide[blank_end] for [blank_start]template[blank_end] strand and builds onto [blank_start]primer[blank_end]
5. label: Sanger suggested dideoxyribonucleotides ([blank_start]fluorescently[blank_end] tagged) modified [blank_start]nucleotides[blank_end] that [blank_start]terminate[blank_end] the chain
End result: [blank_start]lots[blank_end] of copies of [blank_start]different[blank_end] [blank_start]random[blank_end] lengths, labelled with the [blank_start]last nucleotide[blank_end] added, [blank_start]detector[blank_end] reads the [blank_start]fluorescent[blank_end] tags and writes the [blank_start]sequence[blank_end].- Asequencing
- Bsynthesise
- Clabel
- Doriginal sequence
- Esingle
- F5
- G3
- Hone direction
- Isynthetic
- Jligonucleotide
- Kcomplementary
- Lknown
- Mbind
- Ncopying
- Oenzyme
- Pcopy
- Qpolymerase
- Rcomplementary nucleotide
- Stemplate
- Tprimer
- Ufluorescently
- Vnucleotides
- Wterminate
- Xlots
- Ydifferent
- Zrandom
- AAlast nucleotide
- ABdetector
- ACfluorescent
- ADsequence
5Sequencing DNA Today:
We can only [blank_start]synthesis[blank_end] set regions so need to do [blank_start]overlapping[blank_end] sequences and put them back together → this is [blank_start]inefficient[blank_end] so use [blank_start]recombinant[blank_end] methods:
1. Take [blank_start]many copies[blank_end], smash them up using [blank_start]ultrasound[blank_end], end up with [blank_start]overlapping[blank_end] chunks → important that they [blank_start]overlap[blank_end].
2. Use theory of [blank_start]recombinant[blank_end] DNA, [blank_start]ligate[blank_end] [blank_start]synthetic[blank_end] [blank_start]linkers[blank_end] with [blank_start]known[blank_end] sequences to the [blank_start]ends[blank_end] of each fragment
3. Shotgun all the sequences at the same time using [blank_start]primers[blank_end] that [blank_start]bind[blank_end] to the known linkers, computer records the [blank_start]bases[blank_end] that are added to the [blank_start]unknown[blank_end] DNA between the [blank_start]known[blank_end] linkers
4. Computer puts pieces ([blank_start]reads[blank_end]) back together ([blank_start]contigs[blank_end]) like a giant jigsaw puzzle. Ignores [blank_start]linkers[blank_end] and tests each [blank_start]sequence[blank_end] with [blank_start]overlap[blank_end] so tries to make one [blank_start]continuous[blank_end] [blank_start]contig[blank_end].
Challenges:
[blank_start]Mistakes[blank_end] → sequence each genome many times
[blank_start]Computing power[blank_end] → high time/money cost
[blank_start]Repetitive[blank_end] gene sequences → map against reference genome- Asynthesise
- Boverlapping
- Cinefficient
- Drecombinant
- Emany copies
- Fultrasound
- Goverlapping
- Hoverlap
- Irecombinant
- Jligate
- Ksynthetic
- Llinkers
- Mknown
- Nends
- Oprimers
- Pbind
- Qbases
- Runknown
- Sknown
- Treads
- Ucontigs
- Vlinkers
- Wsequence
- Xoverlap
- Ycontinuous
- Zcontig
- AAMistakes
- ABComputing power
- ACRepetitive
6How do we find the genes?
1. ORFs: Computers can look for a [blank_start]TATA[blank_end] sequence within about [blank_start]20[blank_end] pairs of a [blank_start]Met[blank_end] and then 100 [blank_start]consecutive[blank_end] codons ([blank_start]open reading frame[blank_end]) that would code for [blank_start]proteins[blank_end] before a [blank_start]stop[blank_end].
2. Transcriptome analysis: [blank_start]RNA[blank_end] is the [blank_start]DNA[blank_end] that is being actively [blank_start]transcribed[blank_end] therefore get the [blank_start]RNA[blank_end] from a cell, [blank_start]reverse transcriptase[blank_end] to [blank_start]DNA[blank_end], sequence [blank_start]DNA[blank_end] → this is Probably [blank_start]DNA[blank_end] that is being used to make a [blank_start]protein[blank_end]. The sequences are often called [blank_start]expressed sequence tags[blank_end] or ESTs
3. Comparative genomics: [blank_start]Compare[blank_end] to [blank_start]related[blank_end] genome and look for [blank_start]conserved[blank_end] regions.- ATATA
- B20
- CMet
- Dconsecutive
- Eopen reading frame
- Fproteins
- Gstop
- HRNA
- IDNA
- Jtranscribed
- KRNA
- Lreverse transcriptase
- MDNA
- NDNA
- ODNA
- Pprotein
- Qexpressed sequence tags
- RCompare
- Srelated
- Tconserved
7Mutations are a driving force for [blank_start]evolution[blank_end] because they provide [blank_start]variation[blank_end]. The effect of a mutation on an organism can be [blank_start]beneficial[blank_end], [blank_start]neutral[blank_end] or [blank_start]deleterious[blank_end], most are [blank_start]neutral[blank_end]. Effects of a mutation also depends on [blank_start]environmental[blank_end] effects and [blank_start]other[blank_end] genes.
Silent mutations: ([blank_start]no[blank_end] effect on phenotype) may occur in [blank_start]non-coding[blank_end] regions such as intergenic regions and [blank_start]introns[blank_end], may occur in [blank_start]exons[blank_end] but result in the same [blank_start]amino acid[blank_end].
Missense mutations: change an [blank_start]amino acid[blank_end], may have small or large [blank_start]effect[blank_end] depending on how [blank_start]similar[blank_end] the amino acids are and how important to [blank_start]protein function[blank_end]. Normally [blank_start]loss[blank_end] of function or at least [blank_start]reduced[blank_end] function.
Frameshift Mutations: insertion or deletion has the [blank_start]largest[blank_end] effect because they change the [blank_start]reading frame[blank_end] for the rest of the gene normally resulting in [blank_start]premature termination[blank_end] but [blank_start]nonsense[blank_end] in the meantime. [blank_start]Loss[blank_end] of function.
Triplet extension: some genes contain [blank_start]triplet[blank_end] repeats, if too many [blank_start]repetitions[blank_end] it can lead to [blank_start]dysfunction[blank_end] e.g. Huntington Disease or Fragile X.
Chromosomes can also have [blank_start]larger[blank_end] mutation effects: [blank_start]translocations[blank_end] e.g. myeloid leukaemia, [blank_start]inversion[blank_end], [blank_start]aneuploidy[blank_end].- Aevolution
- Bvariation
- Cbeneficial
- Dneutral
- Edeleterious
- Fneutral
- Genvironmental
- Hother
- Ino
- Jnon-coding
- Kintrons
- Lamino acid
- Mexons
- Namino acid
- Oeffect
- Psimilar
- Qprotein function
- Rloss
- Sreduced
- Tlargest
- Ureading frame
- Vpremature termination
- Wnonsense
- XLoss
- Ytriplet
- Zrepetitions
- AAdysfunction
- ABlarger
- ACtranslocations
- ADinversion
- AEaneuploidy
8Monogenic Diseases
Huntington
Symptoms: progressive [blank_start]tremor[blank_end], [blank_start]involuntary[blank_end] movements, [blank_start]neurodegeneration[blank_end]
Onset [blank_start]later[blank_end] in life, [blank_start]no[blank_end] treatment. [blank_start]Autosomal dominant[blank_end] inheritance, [blank_start]expansion[blank_end] of a [blank_start]CAG[blank_end] triplet repeat in huntingtin (HTT) gene. CAG codes for [blank_start]glutamine[blank_end] so protein has long [blank_start]polyglutamine[blank_end] tract, becomes [blank_start]unstable[blank_end] and fragments, clumping together in [blank_start]nerve[blank_end] cells damaging them. Use [blank_start]PCR[blank_end] to determine length of [blank_start]CAG[blank_end] repeat. [blank_start]Normal[blank_end] 10-35 copies. [blank_start]Descendant[blank_end] risk: 27-35 copies. Risk of [blank_start]developing[blank_end] disease: 36-40 copies. [blank_start]Disease[blank_end] develops: 40+ copies. Since it is [blank_start]autosomal dominant[blank_end], if a child tests [blank_start]positive[blank_end], the parent is [blank_start]positive[blank_end] by default which has [blank_start]ethical[blank_end] implications as not everyone wants to know.
Cystic Fibrosis
Symptoms: [blank_start]lung[blank_end] infections, [blank_start]pancreatic[blank_end] insufficiency, [blank_start]absence[blank_end] of vas deferens in males, [blank_start]salty[blank_end] tasting skin. Can range from mild to severe. [blank_start]Severe[blank_end] form has [blank_start]frequent[blank_end] infections, hospitalisations and a [blank_start]reduced[blank_end] life expectancy. Inheritance is [blank_start]autosomal recessive[blank_end]. The gene disrupted in CF is a [blank_start]chloride[blank_end] ion transporter, cystic fibrosis transmembrane regulator ([blank_start]CTFR[blank_end]). Reduced function causes [blank_start]thickening[blank_end] of cell secretions, less [blank_start]Cl[blank_end] in a cell, doesn’t attract enough [blank_start]water[blank_end] which leads to infections in [blank_start]lungs[blank_end]. Many [blank_start]different[blank_end] mutations in CFTR gene can cause CF.- Atremor
- Binvoluntary
- Cneurodegeneration
- Dlater
- Eno
- FAutosomal dominant
- Gexpansion
- HCAG
- Iglutamine
- Jpolyglutamine
- Kunstable
- Lnerve
- MPCR
- NCAG
- ONormal
- PDescendant
- Qdeveloping
- RDisease
- Sautosomal dominant
- Tpositive
- Upositive
- Vethical
- Wlung
- Xpancreatic
- Yabsence
- Zsalty
- AASevere
- ABfrequent
- ACreduced
- ADautosomal recessive
- AEchloride
- AFCTFR
- AGthickening
- AHCl
- AIwater
- AJlungs
- AKdifferent
9Polygenic Disorders
Disorders which [blank_start]appear[blank_end] to run in families but do not follow [blank_start]straightforward[blank_end] inheritance pattern. Families can end up with [blank_start]mutations[blank_end] in [blank_start]multiple[blank_end] genes which [blank_start]increase[blank_end] the risk for a disease. This is generally [blank_start]probabilistic[blank_end] not [blank_start]deterministic[blank_end]. Polygenic disorders involve [blank_start]several[blank_end] genes acting together, sometimes with [blank_start]environmental[blank_end] factors [blank_start]interacting[blank_end] with the genes. We need to understand how gene [blank_start]products[blank_end] function and [blank_start]interact[blank_end], the range of [blank_start]normal[blank_end] variation and [blank_start]environment[blank_end] risk factors. Examples of polygenic disorders: [blank_start]Heart[blank_end] disease, H[blank_start]ypertension[blank_end], some C[blank_start]ancers[blank_end], D[blank_start]iabetes[blank_end], M[blank_start]ultiple Sclerosis[blank_end], B[blank_start]ipolar disorder[blank_end], R[blank_start]heumatoid arthritis[blank_end].- Aappear
- Bstraightforward
- Cmutations
- Dmultiple
- Eincrease
- Fprobabilistic
- Gdeterministic
- Hseveral
- Ienvironmental
- Jinteracting
- Kproducts
- Linteract
- Mnormal
- Nenvironment
- OHeart
- Pypertension
- Qancers
- Riabetes
- Sultiple Sclerosis
- Tipolar disorder
- Uheumatoid arthritis
10Homologous features share common [blank_start]ancestry[blank_end] but not necessarily similar [blank_start]function[blank_end] whereas analogous features share similar [blank_start]function[blank_end] but not common [blank_start]ancestry[blank_end]. [blank_start]Analogous[blank_end] features are the result of [blank_start]convergent[blank_end] evolution whereby two species adapt to [blank_start]similar[blank_end] environments in [blank_start]similar[blank_end] ways thus ending up superficially [blank_start]similar[blank_end] despite [blank_start]not[blank_end] being closely related.
Sequencing ancient [blank_start]humans[blank_end]/[blank_start]humanids[blank_end] can tell us that [blank_start]ancient humans[blank_end] definitely [blank_start]got it on[blank_end] with [blank_start]Neanderthals[blank_end].- Aancestry
- Bfunction
- Cfunction
- Dancestry
- EAnalogous
- Fconvergent
- Gsimilar
- Hsimilar
- Isimilar
- Jnot
- Khumanids
- Lhumans
- Mgot it on
- NNeanderthals
- Oancient humans
11To [blank_start]compare[blank_end] sequences, we [blank_start]line[blank_end] them up, [blank_start]mark[blank_end] each point where the sequence is the [blank_start]same[blank_end], this is called [blank_start]aligning[blank_end]. More [blank_start]differences[blank_end] = more [blank_start]distance[blank_end] = more [blank_start]time[blank_end]. It is [blank_start]hard[blank_end] to know where to start. It is [blank_start]easiest[blank_end] to do [blank_start]closet[blank_end] related species because there are [blank_start]fewer[blank_end] changes and [blank_start]coding[blank_end] sequences are easier to align because they evolve more [blank_start]slower[blank_end] so [blank_start]fewer[blank_end] changes. Genes that are the [blank_start]same[blank_end] between species come from a [blank_start]common[blank_end] ancestor. [blank_start]Synteny[blank_end] is where [blank_start]genes[blank_end] are present in the same [blank_start]order[blank_end] of chromosomes of [blank_start]different[blank_end] species, indicating common [blank_start]ancestry[blank_end]. [blank_start]Blocks[blank_end] of genes are generally [blank_start]conserved[blank_end] through [blank_start]evolution[blank_end] because when [blank_start]chromosomal rearrangements[blank_end] do occur, they are often [blank_start]deleterious[blank_end]. [blank_start]Closely[blank_end] related species have very [blank_start]similar[blank_end] gene order and [blank_start]organisation[blank_end]. So it is not the [blank_start]genes[blank_end] themselves that makes us [blank_start]different[blank_end] but [blank_start]how[blank_end] we use them. [blank_start]In between[blank_end] the genes are sections which tell us [blank_start]how[blank_end] to use the genes and [blank_start]when[blank_end]. The genes are the [blank_start]ingredients[blank_end] and the rest is the [blank_start]recipe[blank_end]. Things in [blank_start]common[blank_end] between species implies shared [blank_start]biology[blank_end]. Things that are [blank_start]different[blank_end] may encode organism specific [blank_start]biology[blank_end]. This can help us to learn what little bits of the [blank_start]genome[blank_end] do.
- Acompare
- Bline
- Cmark
- Dsame
- Ealigning
- Fdifferences
- Gdistance
- Htime
- Ihard
- Jeasiest
- Kclosely
- Lfewer
- Mcoding
- Nslower
- Ofewer
- Psame
- Qcommon
- RSynteny
- Sorder
- Tdifferent
- Ugenes
- Vancestry
- WBlocks
- Xconserved
- Yevolution
- Zchromosomal rearrangements
- AAdeleterious
- ABClosely
- ACsimilar
- ADorganisation
- AEgenes
- AFdifferent
- AGhow
- AHIn between
- AIhow
- AJwhen
- AKingredients
- ALrecipe
- AMcommon
- ANbiology
- AOdifferent
- APbiology
- AQgenome
12Genome sequencing [blank_start]does not tell[blank_end] us the function of genes. The best way to do this is to [blank_start]knock out[blank_end] a gene in an organism and study the [blank_start]phenotype[blank_end]. [blank_start]Naturally[blank_end] occurring mutants are [blank_start]rare[blank_end] so [blank_start]genetic screens[blank_end] are designed to [blank_start]accelerate[blank_end] the rate of [blank_start]mutations[blank_end]. It’s [blank_start]not ethical[blank_end] to do this in humans but is apparently [blank_start]ethical[blank_end] to do so in [blank_start]flies[blank_end] and [blank_start]animals[blank_end] so we study them instead and hope it is [blank_start]similar[blank_end] in humans. Studying [blank_start]mutations[blank_end] will tell us what genes are [blank_start]supposed to do[blank_end]. We can make mutants by treating creatures with [blank_start]radiation[blank_end] or [blank_start]chemicals[blank_end]. [blank_start]Making[blank_end] and [blank_start]analysing[blank_end] lots of mutants is called a [blank_start]genetic screen[blank_end].
[blank_start]Drosophilia[blank_end] are ideal for such studies because they are [blank_start]small[blank_end] and have a [blank_start]rapid[blank_end] life cycle.
[blank_start]Mice[blank_end] are also often used. They are [blank_start]mammalian[blank_end] so more closely related to us and share more [blank_start]biological functions[blank_end] and [blank_start]genes[blank_end], often [blank_start]aligned[blank_end] in the same way, similar [blank_start]immune[blank_end] system. They are also [blank_start]small[blank_end], [blank_start]easy[blank_end] to maintain, [blank_start]breed[blank_end] a lot and produce large [blank_start]littles[blank_end]. There are good resources of mice because they are [blank_start]commonly[blank_end] used so we have [blank_start]inbred[blank_end] lab strains that [blank_start]reduce[blank_end] variation. The [blank_start]disadvantages[blank_end] are that hey are not the same as us e.g. [blank_start]faster[blank_end] metabolism and [blank_start]different[blank_end] physiology. They are [blank_start]expensive[blank_end] to maintain and keep [blank_start]healthy[blank_end] and there are also [blank_start]ethical[blank_end] concerns.- Adoes not tell
- Bknock out
- Cphenotype
- DNaturally
- Erare
- Fgenetic screens
- Gaccelerate
- Hmutations
- Inot ethical
- Jethical
- Kflies
- Lanimals
- Msimilar
- Nmutations
- Osupposed to do
- Pradiation
- Qchemicals
- RMaking
- Sanalysing
- Tgenetic screen
- UDrosophilia
- Vsmall
- Wrapid
- XMice
- Ymammalian
- Zbiological functions
- AAgenes
- ABaligned
- ACimmune
- ADsmall
- AEeasy
- AFbreed
- AGlitters
- AHcommonly
- AIinbred
- AJreduce
- AKdisadvantages
- ALfaster
- AMdifferent
- ANexpensive
- AOhealthy
- APethical
13The Heidelberg screen: creation of a [blank_start]large[blank_end] series of mutants
[blank_start]All[blank_end] cells of a fly could be affected but only [blank_start]germline[blank_end] mutations pass to the next [blank_start]generation[blank_end]. Mutations are generally [blank_start]recessive[blank_end] so [blank_start]three[blank_end] generations are needed to see the effect on a [blank_start]homozygous[blank_end] mutation at one [blank_start]locus[blank_end]. Essentially look for [blank_start]dead[blank_end] flies and then figure out how you [blank_start]killed[blank_end] them. E.g. look for changes to the [blank_start]embryonic[blank_end] pattern and every mutant represents a [blank_start]single gene[blank_end] involved in [blank_start]segmentation[blank_end].
[blank_start]Transgenic[blank_end] animals can be created by isolating the [blank_start]DNA[blank_end] of interest using [blank_start]PCR[blank_end] and introducing it to [blank_start]fertilised eggs[blank_end]. [blank_start]Transgenic eggs[blank_end] then develop in [blank_start]foster mother[blank_end].- Alarge
- BAll
- Cgermline
- Dgeneration
- Erecessive
- Fthree
- Ghomozygous
- Hlocus
- Idead
- Jkilled
- Kembryonic
- Lsingle gene
- Msegmentation
- NTransgenic
- ODNA
- PPCR
- Qfertilised eggs
- RTransgenic eggs
- Sfoster mother
14Knockout mice: we can [blank_start]remove[blank_end] or [blank_start]replace[blank_end] the gene we are interested in by [blank_start]genetically modifying[blank_end] an organism then examine the [blank_start]resulting[blank_end] organism to identify what the gene [blank_start]normally[blank_end] does. These mice are called [blank_start]chimeric[blank_end] and can be created for any [blank_start]gene[blank_end] provided you know the [blank_start]sequence[blank_end] first.
An example: Cystic Fibrosis in mice
The [blank_start]homozygous[blank_end] mice were missing the gene for [blank_start]CFTR[blank_end] and made no [blank_start]CFTR[blank_end] protein, they also [blank_start]die[blank_end] before they are 40 days old. However they were [blank_start]not a good model[blank_end] for the disease in humans because [blank_start]pancreatic[blank_end] disease was not replicated, the males were not [blank_start]infertile[blank_end], they only developed [blank_start]lung[blank_end] disease after [blank_start]long[blank_end] term exposure to pathogens and tended to die of [blank_start]gastrointestinal[blank_end] complications. But it is possible to test [blank_start]effectiveness[blank_end] of drug therapy to treat the [blank_start]common[blank_end] symptoms and [blank_start]gene[blank_end] therapy to [blank_start]repair[blank_end] or [blank_start]replace[blank_end] the damaged protein.
A [blank_start]pig[blank_end] model develops the disease [blank_start]similarly[blank_end] to humans. Comparing the two models has found that the [blank_start]pH[blank_end] of the airway influences the development of [blank_start]lung[blank_end] disease which could lead to new unexpected treatment approaches.- Aremove
- Breplace
- Cgenetically modifying
- Dresulting
- Enormally
- Fchimeric
- Ggene
- Hsequence
- Ihomozygous
- JCFTR
- KCFTR
- Ldie
- Mnot a good model
- Npancreatic
- Oinfertile
- Plung
- Qlong
- Rgastrointestinal
- Seffectiveness
- Tcommon
- Ugene
- Vrepair
- Wreplace
- Xpig
- Ysimilarly
- ZpH
- AAlung
15Embryo begins as a small number of [blank_start]totipotent[blank_end] cells. Embryonic stem cells can give rise to [blank_start]all[blank_end] cell types except trophectoderm ([blank_start]pluripotent[blank_end]). The cells become progressively more [blank_start]differentiated[blank_end] which progressively [blank_start]restricts[blank_end] its fate until it is [blank_start]terminally differentiated[blank_end]. E.g. a [blank_start]control gene[blank_end] myoD is activated, the cell must now become a [blank_start]muscle[blank_end] cell, it then turns on other [blank_start]muscle specific[blank_end] genes and [blank_start]increases[blank_end] transcription of more myoD and [blank_start]muscle proteins[blank_end].
Stem cells can divide [blank_start]without[blank_end] limit, they are [blank_start]undifferentiated[blank_end]. They can give rise to both [blank_start]stem[blank_end] cells and cells which can [blank_start]differentiate[blank_end] into [blank_start]functional[blank_end] tissue cells. Fertilised eggs are [blank_start]totipotent[blank_end]. Embryonic stem cells are [blank_start]pluripotent[blank_end]. Adult stem cells, such as [blank_start]bone marrow[blank_end] cells, usually only give rise to [blank_start]one[blank_end] or a [blank_start]few[blank_end] cell types. Stem cells are important for tissues such as blood and skin which need constant [blank_start]renewing[blank_end].
Adults: [blank_start]Blood[blank_end] stem cells or haematopoietic stem cells are found in the [blank_start]bone marrow[blank_end] and can be used for [blank_start]transplants[blank_end]. [blank_start]Bone marrow[blank_end] also contains mesenchymal stem cells which can develop into [blank_start]bone[blank_end] and [blank_start]cartilage[blank_end], may also be able to renew other tissues through [blank_start]plasticity[blank_end].
Babies: [blank_start]Cord blood[blank_end] banking is common but [blank_start]expensive[blank_end]. These cells are not [blank_start]pluripotent[blank_end] but [blank_start]immature[blank_end] blood stem cells which can be used to treat [blank_start]leukaemia[blank_end] and other blood diseases.
Induced [blank_start]pluripotent[blank_end] stem cells (iPS): reprogramming [blank_start]adult skin[blank_end] cells, currently involves [blank_start]genetic[blank_end] engineering but could be used in therapy in future. Takes [blank_start]fibroblasts[blank_end] from skin of patient and turns them into iPS which are [blank_start]like[blank_end] stem cells.- Atotipotent
- Ball
- Cpluripotent
- Ddifferentiated
- Erestricts
- Fterminally differentiated
- Gcontrol gene
- Hmuscle
- Imuscle specific
- Jincreases
- Kmuscle proteins
- Lundifferentiated
- Mwithout
- Nstem
- Odifferentiate
- Pfunctional
- Qtotipotent
- Rpluripotent
- Sone
- Tfew
- Ubone marrow
- Vrenewing
- WBlood
- Xbone marrow
- Ytransplants
- Zbone
- AAcartilage
- ABBone marrow
- ACplasticity
- ADCord blood
- AEexpensive
- AFpluripotent
- AGimmature
- AHleukaemia
- AIpluripotent
- AJadult skin
- AKgenetic
- ALfibroblasts
- AMlike
16Gene therapy is based on the idea that it may be possible to [blank_start]alter[blank_end] the genetic code of an individual’s cells. It is proposed as a way of correcting [blank_start]single gene[blank_end] disorders e.g. cystic fibrosis. [blank_start]Normal[blank_end] alleles could be inserted into the cells of [blank_start]affected[blank_end] tissue. Gene therapy is best applied to [blank_start]stem[blank_end] cells because they are the source of [blank_start]renewal[blank_end] for cells so will fix all [blank_start]downstream[blank_end] copies. Possibly use [blank_start]retroviruses[blank_end] containing the corrected [blank_start]allele[blank_end] to infect cultured [blank_start]bone marrow[blank_end] cells from a patient then replace the cells.
- Aalter
- Bsingle gene
- CNormal
- Daffected
- Estem
- Frenewal
- Gdownstream
- Hretroviruses
- Iallele
- Jbone marrow
17Clones:
Somatic cell nuclear transfer: Take [blank_start]nucleus[blank_end] out of [blank_start]somatic body[blank_end] cell and transfer it to a [blank_start]fertilised egg[blank_end]. Easier to use [blank_start]embryonic[blank_end] cells because they are less [blank_start]differentiated[blank_end]. The complete genome is present in [blank_start]all[blank_end] cells (except some [blank_start]immune[blank_end] system cells) but during [blank_start]differentiation[blank_end], most cells [blank_start]lose[blank_end] the ability to regenerate the [blank_start]whole organism[blank_end] because it cannot reset itself to an [blank_start]embryonic[blank_end] state. Differentiation causes [blank_start]modifications[blank_end] to the DNA molecule and its histones.
Reproductive cloning: Dolly the sheep was the first mammalian clone. [blank_start]Egg[blank_end] plus mammary gland cell = [blank_start]embryo[blank_end] → transplant into [blank_start]surrogate[blank_end] mother sheep.
DNA makeup of a clone:
Nuclear genome from [blank_start]nuclear donor[blank_end].
Mitochondrial genome from [blank_start]egg donor[blank_end].
No DNA from [blank_start]surrogate mother[blank_end].
Therapeutic cloning: donor [blank_start]nucleus[blank_end] into an [blank_start]enucleated[blank_end] zygote (the same as reproductive cloning), cultured into [blank_start]blastocysts[blank_end] stage. Embryonic stem cells are made from the blastocysts and [blank_start]cultured[blank_end] under various conditions to make [blank_start]different[blank_end] cell types. iPS cells from patients with [blank_start]genetic[blank_end] disease can be used to make cells or tissues for [blank_start]drug[blank_end] testing.
Difficulties:
Japanese scientists have added a chemical called Trichostatin A to the cloning procedure which targets the maintenance of [blank_start]histone[blank_end] modifications to help [blank_start]reset[blank_end] the DNA to factory defaults.
BUT It is very [blank_start]difficult[blank_end] to clone primates and higher level mammals. Many cloned embryos and foetuses [blank_start]die[blank_end] before birth or have long term [blank_start]health[blank_end] effects and die [blank_start]young[blank_end].
Why would we want to clone humans?
Cloning [blank_start]doesn’t[blank_end] reproduce a recreation of a person, just a person who is [blank_start]genetically identical[blank_end] i.e. identical twins are different people.- Anucleus
- Bsomatic body
- Cfertilised egg
- Dembryonic
- Edifferentiated
- Fall
- Gimmune
- Hdifferentiation
- Ilose
- Jwhole organism
- Kembryonic
- Lmodifications
- MEgg
- Nembryo
- Onuclear donor
- Pegg donor
- Qsurrogate mother
- Rsurrogate
- Snucleus
- Tenucleated
- Ublastocysts
- Vcultured
- Wdifferent
- Xgenetic
- Ydrug
- Zhistone
- AAreset
- ABdifficult
- ACdie
- ADhealth
- AEyoung
- AFdoesn’t
- AGgenetically identical
18HIV is the [blank_start]fastest[blank_end] evolving thing we know, so patients don’t have [blank_start]one[blank_end] virus, they have [blank_start]many[blank_end] viral variants, each of which has evolved to be [blank_start]more effective[blank_end] in that patient specifically and evolved [blank_start]against[blank_end] the drugs the patient is on therefore [blank_start]resistance[blank_end] to therapy, even [blank_start]complex[blank_end] therapy arises rapidly. Making effective [blank_start]vaccines[blank_end] is incredible hard. The [blank_start]immune[blank_end] system will learn a [blank_start]virus[blank_end] and become effective against it but cannot [blank_start]recognise[blank_end] something which is constantly [blank_start]changing[blank_end]. Estimates of [blank_start]5x1010[blank_end] cells containing provirus in a patient therefore potentially that many [blank_start]different[blank_end] versions of the virus.
Everything evolves at [blank_start]some[blank_end] speed. Other retroviruses also evolve [blank_start]quite[blank_end] fast, anti-biotic resistant bacteria are also a result of [blank_start]evolution[blank_end]. [blank_start]Evolutionary[blank_end] thinking can help us [blank_start]understand[blank_end] and respond to [blank_start]pathogens[blank_end] like HIV.- Afastest
- Bone
- Cmany
- Dmore effective
- Eagainst
- Fresistance
- Gcomplex
- Hvaccines
- Iimmune
- Jvirus
- Krecognise
- Lchanging
- M5x10^10
- Ndifferent
- Osome
- Pquite
- Qevolution
- REvolutionary
- Sunderstand
- Tpathogens
Informationen
- Beschreibung
- Quiz am Cells Module 3 short, erstellt von Juliet S am 22/05/2018.
- Autor
- Juliet S
- Sprache
- English
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- 0
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