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genetics final
| Question | Answer |
|---|---|
| things under genetic control | cell proliferation, cell specialization, cell interaction, cell movement |
| cell proliferation | how does a small number of cells become a larger number of cells? |
| cell specialization | how do those proliferated cells obtain the instructions they need to specialize? |
| cell interaction | relationship between cells drive these specializations (how the proteins from the previous gene affects how following ones are expressed) |
| cell movement | how do the cells move once theyve become specialized |
| development | series of changes from fertilized egg through maturity and beyond |
| developmental genetics | how do all of the complex changes happen? (plays out via organisms life) |
| anterior | head |
| posterior | butt/tail |
| dorsal | back surface |
| ventral | belly surface |
| what makes animals different genetic material wise? | genetic material is very similar across all animals, but its the PATTERN in which things are expressed that create the changes ex: the ORDER; hella combinations that make hella creatures |
| pattern formation | development each species has its own pattern its forming as it develops (individuals in a species will share patterns) |
| positional information | determining the axis gradient important distinction where we see maternal effect genes? all cells have the potential to differentiate as one or another, but the differentiation is determined by the concentration of a morphogen along a gradient |
| 3 main mechanisms of pattern formation | positional information (gradients; where there's a lot of x will happen and where there's not Y will happen) induction inhibition |
| how is info provided to cells in cell development? | localization of proteins where a certain protein is expressed, protein=morphogen |
| induction | some cells instruct other cells on what to do |
| misplacing of induction cells | can lead to wrong things to grow in wrong places |
| how does one cell tell other cells to do something in induction | a protein, for example one foreign cell is put in neutral cells and shares its protein so they become that type of cell too |
| what do inhibition and induction tell us | cells can communicate with each other via lots of induction and inhibition, we see interesting/complex patterns emerging |
| what controls protein localization and expression from genes? when and where theyre produced | transcription and translation |
| does having the same genes lead to having the same developmental pathway? why? | no timing matters same with order of operations differences in dna sequences, not nevessarily genes; ex: where ehancer sequences are |
| highly related organisms | go through the same early developmental pathways and diverge later in development |
| syncidium | one cell with multiple nuclei seen in development, in egg stage (1st stage) of fly development for example |
| T | thorax |
| A | abdominal |
| life stages of a fly | larva pupa adult |
| forward genetics | observe a phenotype and try and figure out the genetic mechanism for it how we started researching the mechanisms of development genetics; they saw flies with legs on their head and said hmmm howd that happen |
| reverse genetics | manipulating genes and observing phenotype that results |
| bithorax | mutation of flies where they had 2 sets of wings mustve been duplication o gene expression pattern o the abdominal segment that makes wings "mutation that causes 2 thoraxes to develop" signal was changed that told abdominal segment to act like thorax |
| antennapedia | mutation where flies had legs where their antennas were supposed to be! |
| homeotic genes | the genes responsible for making the big changes in body plan at end of development ex: hox control the identity of segments and therefore control what grows out of the segments seen largely as switches for turning on certain patterns of development |
| effect of a small change in a homeotic gene | HUGE phenotypic change can cause huge probs in body plan |
| goal of homeotic genes | maintain normal development pattern "homeo" think homeostatis maintaining normal state |
| hox gene | type of homeotic gene that controls pattern formation its a homeotic gene with a homeobox produces hox protein which affects/controls pattern formation determine the final expression patterns |
| homeobox | hox GENES have it; its what makes them hox shared dna sequence found in hox genes region of VERY high similarity in the sequence of the gene (similar gene seq=similar hox protein products) similar gene dna sequence |
| varieties of hox genes | 8 of them labial (lab) (mouth) deformed (Dfd) sex combs reduced (Scr) (sex combs are bristles on first segment in males that help in courtship) antennapedia (Antp) ultrabithorax (Ubx) abdominal-A (abdA) abdominal-B (AbdB) |
| where are hox genes found | 2 locations on chromosome 3 the bithorax and attenapedia complex "HOX COMPLEXES" diff types of hox genes show up in different segments to cause/ "code for" different things |
| bithorax complex | contains utrabithorax (Ubx), abdominal-A (abdA), and abdominal-B (Abd-B) |
| antennapedia complex | contains labial (lab), deformed (Dfd), sex combs (Scr), and antennapedia (Antp) |
| hox gene mutations (causing bithorax or antennapedia) happen at the end of development. how do we know this? | if it was earlier they prob wouldnt have survived and we wouldnt know about em |
| homeodomain | the equivalent to the homeobox but on the hox PROTEIN shape of hox proteins very similar in the regions/ positions encoded for by the homeobox similar protein shape these proteins grab onto dna and regulates gene expression |
| hox proteins are very much like | repressors need to be there for the genes to be turned off default is that genes are turned off and then hox proteisn are not bound to the gene that needs to be on because the leg need to be made for example, in the abdomen |
| mehcanism of hox proteins | they bind to dna sequene and repress that sequence that will lead to formation of limbs in the abdomen want to derepress then in the thorax, where we want them |
| hox genes are like | an on/off switch |
| hox genes are all very similar in the homeobox region; they are more similar _______ than _________within species | across; within |
| similarity of hox geens across species is good evidence for | common ancestry chances are, like with fruit flies and mice for exampel, they had a shared common ancestor which likely had hox genes and along the line split |
| similar features in hox genes indicate their | importance if it aint broke dont fix it |
| nusslein-volthard and wiesclus | looked at the rest of the toolkit of protein control of development; beyond hox genes |
| toolkit gene | involved in EARLY stages of development (hox is involved at the end of the process) |
| heirarchy of toolkit genes from first to last | maternal effect (coordinate), gap , pair rule, segment polarity, homeotic (including hox) |
| maternal effect genes /coordinate genes beginning | mom makes proteins she deposits in egg these are then localized to specific regions of the egg and these give instructions to developing embryo about needed gradients for axis formation (dorsal, ventral, anterior, posterior) GENES DO NOT EXIST IN EMBRYO |
| maternal effect gradients set up by | genes the MOTHER is expressing the mom has the genes and expresses the proteins which are put into embryo to start the process these genes are inherited by but not expressed by embryo until they become a mother |
| maternal effect/coordinate genes | affect POLARITY of larva (anterior, posterior ventral, etc) ex: biocoid and nanos |
| bicoid | type of maternal effect gene and protein that tells the larva anterior an posterior axis a mutation here will affect that very 1st decision of wheres my head/tail |
| gap genes | first genes actually EXPRESSED by the embryo/developing zygote turned on by maternal effect proteins; the maternal effect proteins tell the gap genes where they should or should NOT be turned on/expressed ex: hunchback, kruppel, giant |
| pair rule genes | turned on by gap proteins build on pattern started by gap genes determine smaller segments within the gaps ex: eve (even skipped, odd skipped) makes segments |
| segment polarity genes | now what we have segments (from pair rule), those segments have to know whats up and down/ left right; orient them "am i the anterior or posterior part of my segment same concept as maternlal effect but on different scale ex: engrailed |
| to know the effect a maternal effect gene mutation will have | we have to look at mom's genotype |
| what does mom put into her egg from maternal effect genes | mRNA which then produces the proteins in the egg technically the proteins themselves not put in |
| posterior system of maternal effect gene | uses localized NANOS mRNA presence of the NANOS protein causes the cells around it to develop into abdominal parts, for example where the nanos is concentrated becomes the poterior part of the fly produces gradient |
| anterior system of maternal effect gene | uses localized BICOID mRNA presence of the BICOID protein causes the cells around it to become the head produces gradient |
| nanos and bicoid can overlap to make a dual way gradient; this gradient: | its proteins act as inducers for gap genes in that region (where they are) to turn on, but only the ones that are supposed to turn on (based on if theyre in the head or tail region) it sets up the anterior posterior axis |
| how does the regulatory/coexpression of maternal effect and gap genes, bicoid and hunchback, for example, happen? | there are binding sites that are binding sites for M.E. protein , M.E. can bind and recruit polymerase and encourage expression of GAP lots of binding of ME protein to GAP binding sites leads to lots of expression of GAP genes therefore GAP proteins |
| what do gap gene mutations lead to | a misidentification of where these large chunks of larva are supposed to be |
| types of gap genes | hunchback giant kruppel knirps |
| Maternal effect genes can be subdivided into | gap genes head, thorax, abdomen |
| gap genes segment into | head parts, thorax and abdomen if one isnt turned on they may be missing head or entire section of abdomen |
| gap genes can be segmented into | pair rule genes |
| pair rule genes | expressed as a repeating element that makes stripes ex: even skipped, which is a pair rule gene that makes all even numbered segments alone larva ex: into a1,a2,a3,a4... |
| mutations in pair rule genes | lead to missing or wrong facing segments |
| segment polarity genes | once the segments are made from the pair rule genes, each one needs to know left and right up and down--these do that ex: gooseberry and patched |
| if a gap rule gene is mutated what is the affect? why? | everything downstream of it will not be activated (gap gene but also pair rule and segment polarity) because all of these build on themselves like ball factory |
| segment polarity genes activated by | proteins from the maternal effect, gap, and pair rule genes all of the proteins from those |
| anything that happens later can be affected by | genes turned on earlier |
| can segment polarity genes affect gap genes | no; because it is activated after |
| a toolbox gene is affected by | all of the genes that came before it, or rather, the proteins from all the genes that came before it think of that graph we worked with a bunch; it was activation of pair rule but it contained bicoid and hunchback; both maternal and gap proteins |
| enhancers | DNA sequences that have the ability to bind the proteins of earlier expressed genes |
| the expression pattern is __________ finely regulated (more complex patterns) the ________ protein products that have been made earlier in development | MORE MORE |
| the 3 illustrated examples were using for fruit flies have to do with: | 1) maternal gradients (maternal effect genes making gradients) 2) Drawing stripes (gap and pair rule genes) (the graph weve been looking at) 3) making segment different (hox) (turning on legs and other appendages) |
| pair rule genes make how many stripes? how many segments? | 7 stripes for 14 segments |
| where should enhancers be relative to the gene they're regulating/enhancing | they can be far away doesnt matter! |
| when are hox input | end of pupal stage |
| -------------------onto population genetics------------------------------- | --------------------------------------------------------------------------------- |
| modern synthesis | 1950s took the work of mendel and merged it with work of darwin and wallace and them to synthesize them into a unified understanding of how genetics and evolution work together |
| population genetics | unified understanding of how genetics and evolution work together OR the study of how genotype and allele freqs change over time and we can attribute these changes to evolutoinary forces like selection, gene flow, genetic drift, and mutation |
| equal segregation | says we can cross a male Aa (heterozygote) and female Aa (Aa x Aa) and 1/2 of their gametes will be A and half will be a we watch equal segregation play out in meiosis when |
| when can you apply mendels rule of segregation to a population | when mating is random and any given individual can mate with any other given individual |
| population genetics is all about | 1) frequencies of alleles in a population and determining: does frequency of GENOTYPES match our expectations given the frequency of alleles of a gene? 2) counting frequencies of 3 possible genotypes @ a gene |
| important conceptual difference between mendellian genetics and population genetics | we arent focusing on individual crosses, were taking totality of all crosses that occur in a population |
| if generation 1 genotypes dont match generation 2 genotypes what happened | evolution |
| when talking about allele frequencies, the main cross is ________ and the progeny is _________________ | the population TOTAL progeny of all the crosses |
| questions we ask when studying allele frequencies | within a species, are there more or less heterozygotes in certain areas? (distribution across landscape) how do these frequencies change across generations? are they being subjected to evolutionary forces that are causing these phenotypic differences? |
| distribution across landscape | how genetic variation is structured, distributed spacially |
| changes in population from generation to generation | temporal changes in genetic variation |
| what are the 4 main evolutionary forces | natural selection, genetic drift, gene flow, mutation |
| the 4 evolutionary forces have potetial to | change both allele and genotype frequencies specifically, the # of each allele in the space we define as the population |
| natural selection | NONRANDOM; allele freqs change for a reason if offspring are selected in a generation, causing decrease in heterozygotes, and second gen undergoes the same selective pressure, well see a further decrease in heterosygotes |
| what can we investigate with natrual selection | we can estimate the strength |
| genetic drift | NEUTRAL evolution no expectation of what alleles will increase and decrease; on average it evens out in any given generation, they do have changes alleles change RANDOMLY , just by luck/chance |
| mutation | any time there is a new mutation in a sequence, an allele is born maybe it changes phenotype and maybe it doesnt, but either way it changes allele frequency (all the other freqs must go down) |
| gene flow | movement of individuals from 1 pop to another example: moving from population of all heterozygotes to all homozygotes, youre distrupting those allele freq changes from 1 gen to the next |
| if the 4 evolutionary forces dont change the expectation is | the allele frequencies do not change the population is at equilibrium if you do an experiment and allele frequencies change, you can assume its one of these |
| gene pool | total genetic info encoded in the genes in a breeding population @ a given time |
| what does the hardy weinberg formula come from | the mathematical probability of encountering these freq. in the wild |
| in terms of heterozygotes and homozygotes, who does better? | heterozygotes because theyre more genetically diverse |
| if allele frequencies are very similar (ex: p=0.5, q=0.5) | you should see lots of heterozygotes can check your math this way! |
| when can you find the allele frequency from a genotype | ONLY if youre explicitly assuming the population is in equilibrium in this case youd take the root of p^2 or q^2 **square root nonsense needs to be linked with the assumption that were in equillibrium** |
| multiple alleles genotype frequencies | instead of 2 ways t be homozygous and 1 to be hetero theres 3 ways to be homo (p2, q2, r2) and 3 ways to be hetero (the 3 possible combos of p, q, and r) bc theres 3 alleles doesnt mean individual can have 3 alleles; they’re still diploid;3 option now |
| hardy weinberg law | states in the absence of evolutionary forces, a randomly mating population has allele and genotype frequencies that DO NOT CHANGE no change from.1 gen to the next means no evolution/no forces @ play |
| hardy weinberg is used for our _______ when testing for evolution | null model |
| if you conclude a generation is in equilibrium how long do they have to stay there | all it takes is one generation of random mating and the 4 evolutionary forces and they’re back in equilibrium |
| how likely is it to find populations in equilibrium | not very lots of conditions to be met to be in equilibrium, and at the least one of the forces is at play |
| positive assortative mating | like individuals mating with like individuals (ex: tall mating with tall, short with short) an extreme version is inbreeding and further selfing |
| inbreeding | most extreme form of positive assortment mating |
| most extreme version of inbreeding | selfing |
| negative assortment mating | similar mate to dissimilar tall to short |
| with nonrandom mating, what changes, if anything | genotype frequencies NOT allele frequencies combination of them change but the actual pool stays the same just shuffling the deck not removing cards the other 4 forces remove cards |
| when do allelic and dentition frequencies possibly shift | if there is significant initial mutation if there is significant gene flow if there is genetic drift if there is selection |
| one measure of diversity | # of different alleles is a measure of diversity ex: if a pop only has 2 versions of a gene (2 alleles), then it has low diversity |
| why is inbreeding genetically bad | it reduces diversity you see more and more homozygous increases the chance that an allele will be brought back to itself (A2) |
| identical by descent | in inbreeding an allele meets back up with itself due to inbreeding event |
| if you inherit a deleterious allele from inbreeding you inherit | the same allele twice from common ancestors its an allele matching back up with itself |
| ultimate source of variation | mutation |
| how much do frequencies change with mutation | very little we usually ignore in pop genetics |
| forward mutation | when the common allele becomes less frequent and rare allele becomes more frequent more likely |
| reverse mutation | less likely when rare allele gets reverted to wt; common allele becomes MORE frequent and rare becomes less frequent |
| neutral mutations | can reach an equillibrium between reverse and forward mutations eventually they’ll be in equal proportions—og and mutated neutral mutation means theres no selection against the allele no survival/evolution advantage or disadvantage |
| gene flow is the result of | an individual moving from 1 pop to another/ leaving its old pop and joining a new one flow is more active than drift; migration; to remember |
| which evolutionary force could be as important as selection | genetic DRIFT |
| founder effect | when a founder event has happened we consider the pop has gone through a bottleneck/restriction |
| we can measure and account for selection if we know | something about the traits and their genetic____success? |
| genetic drift is strongest when | p and q are equal and population is small (small because theres the most oppertunity of change from 1 gen to the next) |
| in genetic drift, when an allele hits a frequency of1 or 0 | it stays there and accumulates no more genetic diversity! |
| neutral evolutionary force | allele frequencies are changing but not with any selective force behind it ; pop not experiencing increased or decreased fitness as a result of change or anything |
| in a graph for natural selection, if selection is not inviting then changes/ variation in allele frequency will be due to | drift |
| what is the best way to explain how we get 2 species from 1? what does this tell us? | allopatry that isolation is a big part |
| immigration/gene flow counteracts | the formation of 2 species from 2 it keeps their gene pools similar |
| species diversity is driven by | patterns of genetic diversity across space and time ex: the hawaiian islands all have different species which match a phylogenetic tree that follows the same pattern of breakage of the islands |
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