2.1-2.3 + 4.4 last part Flashcards
(31 cards)
extensions to mednel single gene inherticance
Bateson coined terms genetics, allele, homoyzgote and hertozygote
certain exceptions to mendelian ratios revealed unexpected pattersn of single gene inhertance
by distilling the signficance of teh patterns, Bateson and otehr extended scope of mendelian analysis to undrstand relationship between genotype and phenotype
dominance isnt always complete
definition fo domiance and receivness depnds on the F1 hybrids that arise from mating between two pure breeding line
if hyprid is identcial to one parents than the allele carried by parent is compeletly dominant to allele carried by the other parent
complete domiance isnt the only type of relatinship between alleles of a gene
croses bewteen true breeding strains can produce hyrbids that differ from both parents
incomplete domiance
flower colour serves as an example of incomplete dominance: heterozygote doesnt resemble either homozygous parent but exhibits a phenotype that is intermediate between those of the pure breeding parents
ex. cross between pure bred red and pure bred white results in hybrids with pink blossoms and then if they cross, it results in a 1:2:1 phenotypic ratio (same as the genotpic)
simple explanation of incomplete domiance is that the A gene specieis protein (enzyme) needed for reg pigment - the white allele A2 doesnt give rise to function enzyme by A1 does - amount of red pigment is prooprtional to number of functiong enzyme molecules - so homozygous A1 produced enough red by in heterozygote A1A2 the one red allele only makes enough pigment to form pink
codominance
cross between pure breding spotted lentls and pure breeding dotted lentils forms heterozygotes that are spotted and dotted
bc the F1 heteroygotes have charcetrics of both parents, the alleles are termed codomiant
self fertlziton of F1 produced F2 with ratio of 1:2:1 for both the phenotype and genotype
bc the heterozygotes cna be distinguished from the homozygotes, the phenotypic and genoypic ratios conincide
in huamns some alleles that distinguish diff blood cells ehxibit codomiance
ex. one gene I with allele A and B control presence of sugar polymer that protrudes from the red blood cell
the alt alleles specify diff forms of an enyzme that produced diff forms of the complex sugar
in heterozygotes indivduals, the red blood cells carry both the A detrmned and B determined sugars on their surfaces whreas the cells of homozygous idivduals display the suagrs dtermined by A or B alone
when both alleles are functional they are often codomiant for traits analyzed at moelcular level
determinations of domance relations depnd of appearence of F1 gen
complete domaince, F1 progeny look like one of the true breeding parent; have 3:1 phenotype ratio in f2
incompelte domaince have a intermediate phenotpe
codiamcne have charcercis of both parents
both of these domaince have 1:2:1 phenotype ratios in f2 gen
mendelian law of segregation still holds
the dominance relations of a genes alleles dont affect the alleles transmiison
whether two allels of a single gene show any tpe of domiance, the domaince dpends on kind of proteins determiend by alleles and the biochem functions of the proteins
the domiance reltions dont impact teh segregation of alleles duirng gameet formation
as mendel prosped, cell carry two copies of each gene and the copies segregate during gamete formation
fetrliztin restores the two alleles withotu refrence to whetehr the allels are same or not
A gene may have more than two alleles
for many traits more than two alleles exist (but a person only holds two)
ex. are traits like ABO blood types, lentil seed coat patterns and human histocompatibilty
ABO blood types:
if person with type A matches with B its possible that the child isnt A, B or AB but a fourth type of O
ABO blood type has three allles: A, B and i
allele A rises blood type A by specifyin enzyme that adds sugar A while i doesnt specify a functinal sugar adding enzyme
A and B are domiannt to i and blood type O is result of homozygous for allele i
combo of alleles AB results in blood tupe AB
a given gene may have multiple alleles; in our example, the series of alleles is denoted by A B and i
even though ABO blood group has three allles, a person caries only two - there are 6 possible genotypes
the law of segregation remains intact: two alleles of a gene seperate during gamete formation
an allele isnt inherintly domainat or recessive; its domaince or recesivness is relative to a second allele - relations are unique to a pair of alleles
mathcing ABO blood types is prereq of successful blood transfusuions bc ppl make antibodies to foreign blood cell molecules - a carries antibodies of b, b carries antibodies of a, ab carries no antibodies, and O produces antibodies of a and b - thats why O is universal donor and AB is universal acceptor
info about BO blood types can be used in legal evdience for patenrity or criminal guilt
lentil seed coat patterns:
lentils offer another ex of multiple alleles
a gene for seed coat pattern has five alleles: spotted, dotted, clear and two types of marbled
reciproal crosses between pairs of pure breeding lines of all patetrns clarfied domaince relations of the pairs of allles
the result reveal a dominace series in which alleles ar elisted in order from most domiant to most recessive
ex. crosses of marbled 1 with either mabled 2 or psotted or dotted or clear produced marbled 1 and ratio of three mabeld 1 to one of any other charcertcis in F2 showing that amrbled 1 is completly domiant to the others
analogous crosses with remaing 4 phenotypes reveal domaince series - domaince relations are menafigcl when comparing two alleles = some patterns yeielded 3:1 or 1:2:! ratio in f2 gen
histocmpatbilty in humans:
in some alllelic series, eahc allele is codamnt with every other allele and every distinct genotype prduces a disticnt phenotyp
this happens with traits defined at moelcular level
ex. is three genes that specify family of related cell surface molecles in humans and other mammals known as histoompatbility antigens
carried by all body cells by RBC and sperm, the antiegns play crcial role in immune response
bc each of the three major genes has 400-1200 alleles the number of combos in a person create huge varitaion that most ppl cant match
bc ppl make antibodies to nonself histocatbility antigens, the extreme variation has consequences during transplant organs - doctors try to get similar matches by using family memebrs bc alleles are siilar and wont be rejected
mutations are source of new alleles
mutations - alterations of genetic material - create new alleles
once they occur in gamete producing cells they are inhertied
mutations happen at low freq
mutations make it possible to follow gene transmisison
if ex. mutatin specifes alteration in enzyme that produced yellow, now prduing green, the new phenotype makes it pssible to recgnzie the muatnt allele
it takes at least two alleles to see transimison of gene
genetcist can anayzle only genes with variants; tehy have no way of follwing gene that only comes in one form
monomorphic genes
bc each organsm carries two copies of a gene u can calc the copies of a gene in a population by mutiing number of indivduals by 2
each allele of gene accounts for percentage of total number gene copies and that percent is known as allele frequency
the most comon allels in a population are called wild-type alleles - have + superscript
allele is wild type if its present in population at frequency greated than 1%
a rare allele is considered mutatnt allele - a newly introducd muyation gives mutant allele whose frequency can inc overtime becoming wild type
ex. in mice agouti gene is main type dterming coat colour
wild type A prduced fur with yellow and black bands that blend giivng dark gray or agouti
there are 14 mutant alleles for agouti gene
one is at recessive to wild type and give black coat
another a is reccive and produced pure black
the AA agouti wild types surive while the mutants are less likely to survive so A is at frquncy of mcuh more than 99% and thus is only wild type alllel in mice for agouti gene
a gene with only one common, wild type allele, is monomorphic
polymorphic genes
some genes have mroe than one common allele making them polymorphic
ex. in ABO all alleles A, B and i have appreciable frqency
all types can be considered wild type but genetics refer to high freq alleles of a polymorphic gene as common variants
some scinetist think that evolution favuurs the emergence of new histocomability genes to ensure that no single pathoegn could desory human population
at least a few indicvual with partcilar HLA genes would be rpoetced form any pathogen
pleiotropy
single gene cotnributing to sevral chacertics
mendel remkaed that specifc seed coat colours are alwasy associated with specifc flower colours
phenomenon of single gene detrming number of distinct traits is known as pleiotropy
bc genetcist now know that each gene dtermines a specific protein (or RNA) that can have a cascade of efefcts on an organism we can undeand how pleiotrpy arises
ex. maori of new zeland, males dveelop rspritory issues and are sterile
these males exhibit syndrome - group of probs that are suually seen together
researcher found that receive aklle of gene causes this
the genes normal domiant allele specifies protein needed for action of cilia and flagella
in males who are homzygous recive, cilia that nroamly clears airways fails to work and flagella that propels sprm also fails
thus one gene dtermines portein that affects both respiratory funtion and reproduction
mutations in almost any gene can have pleiotripic effects bc proteins infleucne many biochem rpocesses
recessive lethal alleles
pleoitropy can obscure mendelian ratios
mendels results de0end on fact that alle pea genotupe were equally viable
but is large percent of homogotes for allele died before germination or birth then the 1:2:1 rato and 3:1 ratio for f2 could be altered
ex. inehrtance of coat colour in mice
the wild type agouti AA have black hair iwth yellow stripe that appear dark grey
one of teh 14 mutant alleles Ay gives rise to mice with almost yellow coliur
when pure breeding AA mate to yellow, offpsirng are in 1:1 ratio - all yellow mice must carry wild tpe A even though they dont expres the agouti phenotype, yellow is therefore domiant to agouti and all yellow mice are AyA heterozygotes
domance and reciveness are deifned iin context of each pair of alleles
even though agouti A is domaint to At and a mutations, it can be recives to yellow coat colour allele
but mating of yellow to yellow procued unsual phnetpic ratio of two yellow to one agouti - never was a all yellow offpsirng prduced so pure breeding yellow mice AyAy cant form
this sugegst that two copies of Ay is fatal
Ay affect two traits: its domaint to A in coat colour but recceive to A in lethality
an allele like Ay that prvebt survival of homozygote is knwn as recsive lethal allele
howver for most recessive allele mutations, the visiblity of the allele is hard
letha; mutations can arise in many genes and as a result, most animals inclduing humans carry some recesisve lethal mutations
the mutatons usually remain hiden unless in homizygous caused by consaguinous matings (mating ebwteen close relatives)
delayed lethality:
we saw death of homozygoutes prenatally; in eutero
with soem mutations the homozygotes can die later on
infants with TaySach disease - after 6 months dvelop symptoms of dteriating nervous system and by age 6 pass away
disease caused by absence of active lysosomal enzyme leading to accumaltion of wate products in nerve cells
recessive alleles causing prenatal or ealry chidlhood letahlity can be apssed onto subseqnt gens by hterozygous carried bc homozygotes pass away
but for late onset disease causing death in adulhood, homozygoyes can pass it one
ex. friedrech ataxia - loss of muscle coordiantion
domiant alleles causing late onsset letahlity can also be transmitted - ex. huntington disease
but lethality caused by domaint allele that causes death in dveelopment, allele cant be passed on
Sickle cell disease demosntantes the extensins to mendelian gentics
sickle cell is result of faulty gemoglobic molecule
hemoglobic composed of alpha and beta each spefied by diff gene: Hba and Hbb
multiple allles:
B globin gene has normal wild type of HbbA that rises to functionalB globin and 400 mutant alleles found
some reuslt in prduction of hemoglobin that odesnt carry o2 effiently
other precnt prduction of B globin
pleiotropy:
the HbbS allele of b globin affects more than one trait
hemoglobin of homozygou HbbSHbbs undergo aberrant transofmation after relaing their oyegn - can cause many symptoms or even anemia (low RBC count)
but HbbSHbbS homozygotes are resitant to malaria bc organism that causes disease cant multiply rapidly in cells that sickle
recessive lethality:
ppl homozygous for HbbS often dvelop heart failure bc of stress on ciculatory system - most die befor early audlthood
diff domance relations:
comparisons of hertzygos carries of sickle cell lalle idnivduals mke it possible to distinguish diff domaince relationships for diff phenotpic aspects of sickle cell
READ IN TEXTBOOK - butt the allels have diff domiance depdnig on what its copared to and what trait you ae lookig at
2.2 extension to mendel for two gene inhertiance
two genes can interact in many ways to determine a single trait like the colour of a flower, seed coat, chicken feather, dog fur etc
in a dihyrbid cross like mendels, each interaction produces own phneotpic ratios
in following ex. the alternate alleles of each of the two genes are completly dominant A and B or recessive a and b
gene name using the symbol for the domiant allele like gene A and protein product of allele A as protein A
additive interactions between two genes can prduce novel phenotypes
a mating of pure breeding tan and gray lentils prduces a brown f1 gen and then an f2 gen containg brown, tan, grey and green - this is in a 9;3;3;1 ratio
this is same as the mendel dihbrid cross - however in mendels the two genes controled two diff traits
the difference here is that the two genes control the same trait: lentil seed colour
this simplest explanation is that the two genes inetract additievly to produce seed colour
for the two genes that detrmine seed colour: both dominant alles must be present to yield brown, the dominat allele of only one gene produces either tan or gray and the complete absence of dominant alleles yeilds green
so four colour phenotypes arises from four genotypoc classes, with each class deifned in terms of the presence of absence of the dominant alleles of two genes
if the domiannce patetrns were incompley or codomiance then the f2 genotypes wouldve given rise to more than 4 phenotypes
how can the 9:3:3:1 pheonype ratio be explained in terms of the action of the proeins by the two genes
the two genes conolling the same trait proabbly function additvely in indepdent biochem pathways - so tan + grey = brown
but only tan, no grey (no B) gives tan
and no tan or grey (no A or B) gives green
epistasis: one gene masks efefct of another
sometimes hwne two genes control a signle trait, teh four mendelian genotypic classes produce feweer than 4 phenotypes bc one gene hides the ffects of another
a gene ineraction in whch one gene masks the effects of another gene is known as epistasis
the gene that does the masking is epistatic to the gene that is being masked (hypostatic)
recessive epistasis
where homozygosity for a recessive allele of one of the genes hides the efefct of a second gene
when a individual is homozyhous for the epistatic recessive allele of the first gene, the phenotype is indepdnet of the allels present at the second (hypostaic) gene
yellow labrador retreivers:
these dogs are inbred meaning tha all indivduals are homozygous for breed specific alleles of most of their genes
however these dogs can be black, choc brown or yellow
alterntaive alleles of two indepdently assorting genes (E and B) control the coat colours
when the domiant E allele of the first gene is present, the B allele of the seocnd gene dtermines black and the bb homozygote is choc
however the ee genotype hdes the effect of any combo of gene Bs alleles to yield yellow
thus the ee is epistatic to any allelic combo at the hypostatic gene B
crosses between pure breeding black retreivers BB EE and one type of pure breeding yellow retrievr bb ee create and F1 gen of dihyrbid black retreivers BbEe
crosses betwene the f1 dihyrbdis produces an F2 gen with nine black dogs B-E-, three brown bb E- and four yellow –ee
only three phenotypic classs exist bc ee genotpic both produce a yellow phenotype
the ratio fo recessive epistatsi in F2 gen is 9:3:4 with 4 being a combo of 3 B-ee and 1 bbee
bc the ee genotpe masks the infleucne of otehr gene, you cant tell whetehr the genotype for the otehr is B- or bb
all coat colours in dogs come from two pigments: dark pigment called eumelanin and light called pheomelanin
when dog has at least one copy of E, protein E ensures that animal makes only eumalenin (no light can be produced)
the protein that is produced by b allele is less effcient than B which is why E-bb have choc coloured
in absence of E protein meaning ee genotpe, only pheomlenain syntehsied so dog is yellow
thats why ee is epistatci to both alleles of gene B: in ee, no eumelain is present so dogs are yellow regardless of being B- or bb
bombay phenotype in humans:
an understanding of recessive epistasi made it possible to resolve an intriuing puzzle in human genetics
in rare isnatnces, two parrents who appear to have blood type O and predicted genotype ii produce child with either A or B
this occurs bc extreme rare trait called bombay phenotype that resembles blood type O
this arises from homozygosity for a recessive allel (hh) of a seond gene that amsks the effects of any ABO alleles that might be present
red blood cell surface mlecules detrmine blood type
type A have enzyme that adds polysacharide A onto sugar subsatnce H; type B has altered form of enzyme that adds B onto sugar H; type O make neither A or B enzyme so have exposed H in membranes
A,B or O carry at least one domiant wild type H allele and thus produce substance H
in bombay pheontype indivduals with hh genotyep dont make H at lal so even if they have enzyme that can add A or B the enzyme has nothing to add it to; so the person appears to be O
homozygosit for recessive h allele of H substance gene masks effects of the ABO gene making the hh genotype epistatic to any combo of A, B or i alleles
person who has hh but has A, B or AB can transmit the A or B allele to gamete and offspring can end up having A or B but one dominant H allele presenting as A or B even though both parents seem to be O type
white sweet pea flowers:
Bateson codncted cross between two lines of pure breeding white flowered and f1 gen were purple
self polination of novel hybrids resulted in 9:7 ratio of purple to white in f2
the two genes work in tandem to produce purple sweet pea flowers and dominat allele of each gene must be present to get the purple
bc it takes two enzymes catlyzing bio chem rxns to change a colourless precrusor into purple, only the A- B- genotpic class which produces active forms of each enzyme can generate purple flowers
the three other genotpic classes where homozygous recessive of one or the other gene or both doesnt result in purple so they are white - the 7 part of ratio encomapses the 3:3:1 part of the f2 ratio
the 9:7 ratio is the phenotpic signature of this reciprocal recessive epistasis in which the dominan allels of two genes acting together produce charcertic while the other genotpes dont
given that the phenotpe potentially associated with either allele A or B is purple then aa is epistatic to B and bb is epistatic to A
if sweet peas are either aa or bb then flowers are white regaldess of if they have the dominant allel of the otehr gene
dominant epistaiss
epistatsi can also be caused by a dominant allele
depdening on the details of the biochem pathway involved, domiant epistasi can result in any one of three diff pheotypic ratios
squash fruit colour:
in sqaush two genes ifnelucne the colour
with one gene, the dominant allele A- dtemines yellow while homozygotes for the recessive allele (aa) are green
a seocnd genes domiant alle (B-) prduces whie whille bb can be eitehr yellow or green, depding on genotpe of gene A
the presence of B hides the affect of A- or aa, producing white fruit and B- is thus epstaic to any genotpe of the A gene
the recessicve b allele has no affect on the fruit colour dteermined by gene A
epistasi in which the domiant allele of one gene hides the ffects of another gene is called dominant epistasis
in cross between whit ef1 dihyrbids the f2 phenotypic ratio is 12 hite: 3 yellow and 1 green
the 12 includes genotpe classes: 9 A-B- and 3aaB-
a biochem pathway undelrying the 12:3:1 phenotpic ratio is shown
chicen featehr colour:
a diff ratio idnicating domiant epistais is seen in the feather colour of certain chcikens
white leghorns have a doubly domiant AA BB genotpe for feather colour; white are homozygous recessive for both genes (aa bb)
cross between the two breeding white strains produced all white dihbird (AaBb)
but in f2 gen there is colour and its a ratio fo white 13 to colour 3
can explain this by assuming domiant epistaid in which B is epistatic to A; the A allele procues colour only in absence of B and the a,B and b alleles produce no colour
interaction is chatcetrized by 13:3 ratio bc the 9A-B-, 3aaB- and 1 aabb give white phenotype
maize leaf development:
in maize two genes A and B conrol leaf development
normal broad leaves dvelop as long as either domiant A or domiant B allele are present
but is no domaint allele (genotpe aabb) then its skiny bc too few cells
given that leaves are malformed only in absence of both A and B the f2 phenotypic ratio is signfying recpirocal domaint epistasi is 15:1
the domiant A allele is epsiatic to bb and domiant B allele is epsuatci to aa
this pattern of inehrtance is due to redunant gene action
the proetins A and B specified by domiant alleles act in paralele, reduent pathways that recruit precursor cells to become part of the leaf
that is if eitehr pathway functions, leaves dvelop normal shape
in most cases the redudnant genes specify nearly idnetcal proetins that eprform same fnction
redundent genes often arise by chance evlutionary proceses that duplicate genes
pooints of epistasis
epsistasi is interaction between allels of diff genes not between alleles of the same gene
recessive epsiatsi usually idnicates that teh domaint allels of the two genes function in same pathway to achiev a common outcome
ex. in labradors the B and E both fucntion to generate black hairs
dominant episatsi usually dincates that domaint alleles of the two genes have antagonisc functions
both in cases of squash and chciekn the domaint allele of gene B prevents depsoion of pigemnt whose syntehsis depdns on domaint allel of gene A
reciprocal domaint epistasis usually means that the function of the two alleles are redundant
ratios
the 9:3:3:1 of teh ofur mendlain genotypic classes in f2 gen can rpduce vairous phenotypic ratios dpending on nature of allele and teh wayy in which the genes inetract through biochem pathways
result can be four, trhee or two phenotpes
additive: 9:3:3:1 ratio
recessive epistatsis: 9:3:4 ratio
recpiprocal recessive epistasis: homozygous recive allel of each gene masks teh domiant allel of the otehr genes: 9:7 ratio
dominant epistais 1: domiant allel of one geen hides efefcts of both alleles of the other gene: 12:3:1 ratio
dominat epsusi 2: domiant allele of one gene hides efefcts of dominant alle of other gene: 13:3
reciprocal domaint epistais: domaint alle of eahc gene masks teh efefcts of recessive allel of other gene: 15:1 ratio
wild type and mutant allels of genes partcoaping in many diff types of biochem pathways can rpduce any specific f2 phenotpic ratio
so if u obsevr a certain ratio in a cross you cant infer the pathway
but if u know pathway biochem and function of the alleles you can predict the phenotpic ratios
incompelet or codmiance can expand phenotpic variation
whne two genes inetract, the four genotpci classes can result in two, three or foru phenotpic classes
we assumed taht there was complete domaince
but for any type of gene ienrtacion, the alles of one gene or both can exhibit complet or incoplete domiance and this increases potential for phenotpic diverzitu
none of the obsrved departurs from mendial phenotpic ratios contradict the gentic laws of segrgation and indepdent assortment
the two alles of each gene still segregate and the two genes still assort indepdntly
lous heterogeity: mutations in any one of sevral genes can cause same phenotype
close to 50 diff genes have recessve mutant alles that can cause deafness
many genes genrate dvelpmental pathways that bring abt hearing and loss of function in any part can result in deafness
it takes a dominant wild toe allele at each gene to produce normal hearing
deafness is a hetogenous trait: mutation at any one gene can give rise to same phenotpe
evidence for locus hetergeinty in human pedigrees:
careful examination of many family pedigrees reveal whetehr locus hetrogeinty - proerty of trait where muyations in any one of two or more genes results in same mutant phenotype - exp;ains inhertcance pattern of trait
in case of deafness - whether partcualr parents who are deaf have reccive muations in the same gene or diff ones can be detemrined by obsrving their children
if children can hear parents likely have muatin in two diff genes, and child carry one normal alle for each geen
but if all chidlren are deaf its liely that both parents are homozygous fro a recessive muattion inthe same gene and all their children are homzygous for the same muation
complemnation and complementation tests:
method for disocevring whetehr a partcular phentpe arises from muatons in the same or diff gene is natrally occuring version of complemnattion test
when what appears to be idnetcial recessive mutant phentpe arises in two sperate breeding lines, gentcis want to know whetehr mutation in same gene are responible for phenotupe in both line
they answer by mating affeced indivduals from two line
if offpsrng reciing two muatons hvae the wildtype phenotype, complemtation occured
observation of compelmation means that the origanl mutations affected two diff genes and for both genes, the normal allele from one parent can provide what the muatnt allel of same gene form the otehr parent cannot
this implies that trait must be heterogenous
the concept of copelmation - where eahc parent rpovides functional allele of a gene that other paent lacks - is. only meangfil is muant alleles are nonfnctional and recessive
in deafness pedigree, all chidlren of two parents who were deaf had nromal hearing shows cmplemnation (AA bb + aaBB gives AaBb and heairng)
2.3 Extension to mendel for complex trait inherticance
the inheritance of many traits appears to be more complex than can be explained by the partciaption of only one or two genes in patterns compatible with straightforward mendlian princples
a reason for compelxity is that more than two genes can finelucne certain traits
a second reason is that egnes arent the only players: the envrimnt and chance can sometimes exert considerable effects on traits that are also geneticaly determined
complex traits are traits detrmined by seevral diff genes and or by the inetraction of genes with teh envrinment
same genotype doesnt produce same phenotype
sometimes even though genotype is present, exepected phenotype doesnt appear
other times, the charcertic caused by genotype does appear but to varying degrees in an indivdual
factors that alter the phenotypic expression of genotype include modfiier genes, the envrinment and chance - these facyors complication the inetrpestion of breeding experiments
penetrance and expresivty
retinoblastoma arises from domiant mutant allele of a single gene but only 75% of ppl who carry mutant allele devlop disease
geneticst term penetrance to describe the prorption of indivudals with a partciualr genotype who show the associated phenotype
penetance can be 100% or complete like mendel stydies or incomplete like retinobalstoma - where its 75%
in some ppl with retinolastoma, only one eye is afefcted while in others both are affected
expresisvty refrs to the degree or intensity withw hcih agenotype is expressed in a pehnotyoe
expresivty can be variable like in retinoblastoma or unvarying
incompelte penetacen and variable expresivty can be a result of chance or by otehr genes and/or the envrinment that casuse variation in phenotypes
