1.3, 2.1(sickle), 3.1, 4.1 Flashcards
1.3 Mendelian Inheritance in Humans
although many human traits run in families, most dont show a simple mendlian pattern of inheritance (ex. eye colour)
like eye colour, most common and obvious human pheontypes arise fromn the interaction of many genes
in contrast single gene traits in ppl usually involve an abornamilty that is disabling or life threatning
ex. are the progressive neurological damage of huntingtons didease and clogged lungs and potential respiratory failure of cystic fibrosis
a defective allele of a single gene gives rise to huntingtons diease; defective alleles of a diff gene are responsible for cyctsic fibrosis
there are 700 thousand single gene or mendial traits known in humans
the allele that causes huntigtons is dominant and the nomral (non disease) allele is recessive
the oppsoite is true for cystic fibrosis - disease cuasing allele is recesisve and normal is dominatn
pedigrees aid the study of herediatry traits in human families
determining a genetic defects pattern of transmmission isnt always an easy task bc ppl make slippery genetic subjects
their generation time is long and the fmailies they produce are small which makes statiscal analysis diffcult
humans dont base their choice of mates on purely genetci considerations and no controlled matings are poossible
geneticist circumvent these difculties by working with many families or sveral gens of a large family
in this way they can study the large numbers of genetically related inviduals needed to establish inhetiance patterns of specific traits
a family histroy knonw as a pedigree is a diagram of a familys relevant genetci features extending back through many gens as possible
from systematic pedigree analysis in the light of mendels laws, genetcisist can tell if a trait is detemriend by altenrtaive alalles of a single gene and whetehr a single gene characetrics is domiant or recessive to its altenrtaive characetricisc
squares rep males, circles rep females and diamonds indicate that sex is unspecified
familty memembers affect by teh condition in question are idncated by a fileld in symbol
a single horizontal line connecting male and female reps mating
a double connected line designates consanguineous mating mening mating between close genetic relatives
horizonatl line above a series is children of same parents arranged left to riht in order of birth
in this case male is production of sperm and famel is production of eggs - looking at biological sex
to reach a conslucion abt the mode of inertiance of a family trait, huamn geneticst must use a pedigree that supplies sufficent info bc with less info the pedirgee can be inetrpreted in multiple ways
several kinds of additional info can help resolve incertainty
human geneticst want to know the frequency at whcih the ttait is found in the population from which the family came
if the disease is rare then the allele giving rise to the disease should also be rare and the hypotehsis would require that the fewest genetcially unrelated ppl carry the allele
need lots of info in a pedigree
we look at extensive pedigrees for the dom trait of huntingtons and reccive condition of cystic fibrossi
the patetrns by which these traits appear in pedigrees prpvide improtant clues that can idnciate modes of inhertance and allow genetcists to asisgn genotypes to family memeerbs
vertical pattern of inhetrance idnicates a rare dom trait
huntignttons disaese is named for Huntignton a physician who first descirbed the course
it shows up in middle age and progresisvly impacts the person
intelluctak deterioriation, depression etc all result from proessive death of nerve cells
if one parent has symtopms, each child have 50% of deevloping it
bc symptoms arent at birth and manfiest later, the diease is known as alate onset genetci trait
proceeding to assignn genetypes in pedigree:
you first need to find out if the disaese causing alelle is domianntt or receissve to the normal allele
several clues sggest that the huntiggton disease is tarnsmitetd by a dom allele of a single gene
everyone who develops it has at least one parent who shows the trait and in several generations, approx half offpsring are affected
the pattern of affected inviuals is vertical: tracing back to ancestors you would find at least one person affetced each gen gving a continus line of ppl with disease
when a disease is rare in the population as a whole, a vertcial pattenr is tsrong evidence tht a dom allele causes the condition; the altenrative would require that many unrelated ppl carry a rare reccsive allele (rdcessive trait that is common might also show up in every gen)
in tracking a dom allele through a pedigree you can view every mating between an afefcted and an unafefcted partenr as analgous to a testcross - if some of offpsring dont have disease then u know the aprent with the trait is a heterozygote
human genetcist use diff symbols than mendels ofr alleles of genes
in human genotypes, all alleles are written in uperacsse
if allele specifies normal fucntion gene product then it has a superscript +
allels that specify no gene product or absnromal sometimes have no sueprcsirpt at all or have a superscript other than + that signfiies a partciualr type of abnormal gene
the gene that causes huntigntons has been dinefies and studies at moelcular level
the protein product of huntingtons is called huntingtin or Htt is needed for proper phsyclogy of nerve cells but the proetins rpecise role in tehse cells inst yet undertood
the domiant disease allele HD specifies a defective Htt protein that oevrtime damages nevre cells
the disease allele is domiant to the nromal alelle bc the presence of the normal Htt protein in heterozygotes odesnt prveent the abornaml proetin from damaging cells
note that this epxlanation for the disease alllee is only one of many moelcular mehcnisms that may result in a disease allele that is dom to the normal alllee of a partcular gene
no treatment exist rn and bc the late onset there wasnt a way fro children to know they carried the disease
most ppl with disease allele are HD HD+ heterozygotes so children have 50/50 chance of inerting and before they are diagnosed a 25% proability of pasisng the defdctive allele to tehir children
with new knoledge of the gene, moelcualr genetcist developed DNA test that dtemrine whetehr an dinvual carries HD allele
if test shows presence then parents might choose to conceive using in vitro fetrlization tech that allows genetyping of embryos - only embryos lacking HD would be introduced into the womb
a horizontal pattenr of inherticane indicates a rare recessive trait
most confiemd single gene dieases are caused by recesive allele
one reason is that with exception of late onset traits, deletrous domiant alleles are unlikely to be trasmitted to the next gen
in contrast indivduals can carry one allele for a recesive disease without ever being afefcted by symptoms
cystic firbsosi common recesive disease in white children
double dose of recesisve CF allele (no CF+) causes disorder which causes mucuous to clog in lungs and organs
important featurs of cytsic fibrosis pedigrees:
frist the family pattenr of ppl showing the trait is hroizontal: parents, grandparent and grandpearent of children with cystic fibrosis dont manfiest the disease while siblings in a single gen may
a horizontal pedirgee pattenr is a strong dincation that the trait is recesisve
the unaffected parents are heterozygous carries: they bear a dom normal allele that masks the effects of the receisve abnsormal one
the seocnd feature of cyctsic fibrosid pedigrees is that many of ocuple who produce affected chidlren are blood relatives(double line)
of course hcildren with cystic firbsosi can have unrelated carier parents but bc relative shar egenes, tehir fopsirng have greater than avg chance of getting two copies of rare allele
carrier parents are both hertozygoes so chidlren have a 1/4 chance of having the disease
a mating between unrelated. carried can produce a child with the didase - how likley is this - the answrr depnds on gene and that partciualr population into which a person is bron
incidence of disease and thsu frqency of carriers varies markedly among populations
the areas of gentics that anylzes differences among groups of indivduals is called popylation genetics
genetic researcher ID’d cystic firbsois gene after huntrigoons
the nromal CF+ makes a proetin called CFTR and this forms a channel in cell membrane that contorl flow of cl- ions through lung cells
the recive CF disease alelle eitehr rpoduces no CFTR or nonfucntion or less functional versiosn of teh protein
bc of osomiss wter flows into homzygous CFCF lung cells that lack the chancell while a thick musuc buiodlson the outside of the cells
phsycians have tried deblitating symptoms with gene therapy (introduing normal gene) but iwthout sucess rn
despite failure of gene tehrapy, idnifctain of the geen repsonsible for the disease has led to efective treatment ofr the dieseae in patients with defefctive alleles
in 2019 FDA approved drug cocktail which ehlps the dfective form of CFTR speifcied by comon allee to function properly
ppl see it as a breakrthoygh bc 90% of ppl are helped
dom or recciev trait in pedigree
dom:
- affected childrne always have at least one affetced parent
- dom traits show vertcial pattern of inhetrance (trait in every gen)
- two affected parents can produce unaffect chidlren if both are hertozygote
recessive:
- affected inviduals can be chidlren of two unaffected carries usualiy resulting of consanguinous matings
- all the children fo two afefcted parent should be affected
- rare recive traits show hroziontal pattern of inehrtance: the trait first appears in one or more memebrs of one gen and is not seen in earlier gens
- receesive traist may show a vertcial pattenr of inehrtance if the trait is extremely common in the population
2.1 Sickle Cell Disease Illustrates Many Extensions to Mendels View of Single Gene Inheritance
Sickle cell diease in humans is the result of a faulty hemoglobin molecule
hemolglobin is composed of two types of polypeptide chains, alpha and beta globin, each specified by a diff gene: Hba for alpha and Bbb for beta
normal rbc are packed with hemoglobin moelcules each of which pick up o2 in the lungs and transport it to body tissues
Multiple alleles:
the beta blobin gene has anormal wild type allele HbbA that gives rise to fully functinal Bglobin as well as close to 400 mutant alleles that have been identified
some of the mutatnt alleles result in the production of hemoglobin that carries oxygen inefficently
other mutant alleles prevent the production of beta globin casuing a hemolytic (blood detsroying) disease called Bthalassemia
we dicuss most common mutant allele of beta globin gene HbbS which specifies an absnormal polypetide that causes sickling of RBC
Pleotropy:
the HbbS allele of the beta globin gene affects more than one trait
hemoglobin moelcules in the RBC of homoygous HbBSHbbS indivduals undergo an abberant transofrmation after releasing their oxygen
instead of remaing soluble in the cytosplasm they aggregate to form long fibers that deform the RBC from a normal biconcavce disk to a sickle shape
the deformed cells clog small blood vessls reducing oxygen flow to the tissues and giving rise to muscle cramps, shortenss of breath etc
the sickles cells are also fragile and easliy broken leading to a low RBC count or anemia
on the pos side HbbSHbbS homozygotes are resistant to malaria bc the organism that causes the disease can multiply rapdily in normal RBC but not in cells that sickle
the infection causes sickle shaped cells to break down before malaria can multiply
recessive lethality:
ppl who are homozygous for the recessibe HbbS allele often devlop heart failure bc of sterss on the ciruclaory system
this causes death uuaally before or during early adulthood
diff dominance relations:
compairsons of heterozygous carries of the sickle cell alelle indivduals whose cells contain one HbbA and one HbbS with homozygous normal and homozygousdisease indivduals make it possible to distinguish diff domiance relationships for different phenotypic aspects of sickle cell disease
at the moelcular level the prodcution of beta glbin proteins both forms of beta globin are present in heterouzgotes so HbbA and HbbS are codominant
at the cellular level in their affect on RBC shape the allels show either complete domiance or codimance depending on altitude
under normal oxygen conditins the great majority of heteroyzgotes tbc have the nromal bicocnave (A domnian to S) whne oxygen leevls drop sicking cells occur in some cells (co dom)
condiserng the trait of reisstance to malalrai, the HbbS alelle is dom to A
infected A/S cells are resitant to malaria bc they break down before malrial organsims has chance to reproduce like the homozygou S disease cells
the HbbS is recessive to A for anemia or death
thus for the beta globin gene as for all genes, domaince and recesiveness arent an inehrtent quality of alleles in isolation; rather they are specific to each pair of alleles and to the level of phsycilogy at whch the phenotype is examined
when dicsusing domaince relatiosnhips its therefore essential tod efne carefully the traits under analysis
in areas where malaira in endemic heterozygoest are betetr at surving and pass on their genes than any type of homyzgote
3.1 Chromsomes: the carrier of genes
mendels insights depended on the idea that genes could be transmitted between egenrations
he assumed that genes were soemhow packaged into the gamates - egg and sperm- and that each must contribute half of the gentic material for making a new progeny
but where in gamets are genes found?
genes reside in nucleus
microspcopist studying fetrlization in frogs and ssa urhcins observed the union of male and female gamtes and recoreded the details in a series of drawings
these drawings and later micrographs show that egg and sperm nuclei are the only elements contributed equally by maternal and paternal gametes
this observation implies that something in the nculeus contains hereditary material
in humans nuelic are less than 2 millionth of meter
genes reside in chromsomes
further investigations dependent on tech innovations in microscopy suggested that smaller discrete tsructures in the ncuelus are the repository of genetic info
in 1880s dyes revealed teh existence of long thereadlike bodies within the nucleus we call chrosmomes
it was now psosible to follow the mvoement of chromsomes during diff kinds of cell division
in embryonci cells the chromsoaml trheads split lengthwise in two just before cell division and each of the two newly fomring duaghter cells receives one half of every split thread
the kind of nuclear division followed by cell divison that results two duaghter cells conating the same number and type of chromsomes as the orginal parent cell is cllled mitosis
in cells that give rise to gamates, the chromsomes composing each pair become segregated so the resulting gamtees only receive one chromsome from each pair
the kind of nucelar division that generates egg or sperm cells ocntanng half the number of chromsomes ofund in the somatic (body) cells is called meisosi
Fertilization: union of haploid gamtes to produce diploid zygotes
cytologists - scitensist who use the micrscope to study cell strcuture- showed that the chromsomes in a fertlized egg consist of two matching sets, one contirbuted by the maternal gamete and the other by the paternal
the corrpsoning maternal and patenral chromsomes appear alike in szie and shape forming pairs (except the sex chromsomes)
zygotes and other cells carrying two matching sets of chromsomes are diploid
gamtes of a diploid organism are called haploid
the number of chromsomes in a gamete is designated by symbol n
the number of chromsomes in anormal diploid cell is 2n (haploid is just n)
in drosophila (fruit fly) they have 2n = 8 and n=4 while humans have 2n = 46 and n=23
halving the chromsome number during meissi and gamete formation followed by the unipn of two gametes chromsomes at fetrlization mromally allows a constant 2n number of chromsomes to be maintained from gen to gen
the chromsomes of eveyr pair must seperate from each other during meisis so that the haploid gamets will each have one compelet set of chromsomes
afetr fetrlziation forms the zygote the process of mitsis then ensures taht all teh somatic cells of cevloping inviduals has identcial diploid chromsome sets
species variations in the number and shape of chromsomes
scientsist analyze the chromsoal makeup of a cell hwne the hcromsomes are most visible at a moemnt in cell cyle of growth and division just before the nucelus divides
this is metaphase - indivdual chromsomes have duplicated and condensed from thin trheads into compact rodlike strcutures
eahc chromsome now consists of two idnetical halves known as sister chormatids
the specific location at which sister chromatids are attached to eachother is called the centromere
each sister chormatid has its own centromemre but the duplicated chromsomes, the sisters are pulled togetehr so tight they form a constiction within which the two centromeres cant be resolbed from each otehr
geneticist often descrbe chromsomes according to the location of the centromemre
in metacentric chromsomes, the centromere is more or less in the middle
in acrocentric hcormsomes, the centromere is close to one end
chromsoems thus have two arms seperated by a centromere by the size vary
cells in metaphase can be fixed and stained with dyes that produce charcertci banding patterns made up of lighter and darker regions
chromsomes that match in size, shape and banding are homologous chromsomes or homologs
two homologs of each pair contain the same set of genes althogh they may carry diff alleles
the diferencs in allele cocrus at molecular level and dont show up in microscope
non homologous chromsomes carry compeletly unrelated sets of genes
to tsudy the chromsomes of a single organism, genetcist arrange micrographs of the stained chromsomes in homologous pairs of dec size to produce a karyotype
theres 46 chromsomes, 22 matching pairs and 1 non matching
the 44 chromsomes in matching pairs are known as autosomes
the two unmatched are sex chromsomes (xx or xy)
karyotypes can reveal misisng or additional chromsomes, a condition called aneuploidy
modern methods of DNa analsyis can rveal differnces betwene the maernal and paternal chromsomes of a homologous pair and can track the orgin of the extra chromsome 21 that causes down syndrom
in 90% of cases 3rd chrosomes 21 comes from egg and frequency inc with female age
Prenatal gentci diagnosis
with new tech for obsevring chromsomes and DNA in genes, doctors can dtermine befor ebirth whetehr fetus has a gentic disorder
the methods dveeloped first were to obtain fetal cells whose chromoes and DNA could be analzyed for genotype
for many years, the most freq used method for aquiring the cells was amniocentesis
doctor insetrs needle into prge womans abdominal wall into amniotic sac in which 16 week fetus grows - the doc withdraws aminitic fluid into syringe - the fluid contains living cells that were shed by fetus - when placed in culture meidum, the cells undergo mitiss - once enough cells availble, clicnians karyotype the chromsoems to learn wheter the fetus is trisomic from chromsome 21 or if it has other abnrmalties
sicnitsits are now able to analyze the gentype of fteussi using motehr blood only
this is possible bc fetal cells leak into the mothers bloodstream and then rbeak dwon reelaisng their dna
genetcist analyze the DNA to dtermine if theres an extra copy of chromsome and to learn the sex of the fetus through presence or absence of y chromsome DNA
such noninvasive prenatal testing is repalcing amniocentsis bc draiwng up blood is enexpesinve, non invasive, and cant harm fetus
it also can be performed at 10th week of preganncy
mdoern dna tech allow sicnetsist to look not only at the set of chromsomes in teh fetus but also to genotpes fetal dna obtaiednfrom amniocnetsis or NIPT for patrcilr disease associated with alleles
in many cases fetuses entire genome sequence can be detrmined
before aminicnetsi was resrcted to age 35 or above bc tehir inc risk of extrachrosme fetus and there was risks and costs with rpocess
but NIPT is inexpensive that its almost a routine screening procedure udirng pregnancy
species variations in the number and shape of chromsomes (contd)
through thousands or karyotypes on nromal indivduals, cytolgist have verified that the cells of each species carry a distincve diploid number of chromsomes
ex. mendels peas carried 14 chromsomes in 7 pairs in each diploid cells, fruit fly drosophila carry 8 chromsomes (4 pairs), ppl have 46(23 pairs)
differences in the size, shape and number of chrosmoems reflect the complex evolutionary histroies of diff species
but the number of chromsomes doenst correlate with teh size or compelxty of an organism
4.1 Sex chromosomes and sex dtermination
Stevens was the first cyologist to show defintely that chrosmomes detrmine sex
examining teh chrosomes in somatic cells of the flour beetle, she notcied that the cells of females contained 20 large chromsomes while those of males had 19 large and one small one
these observations led stevens to exmine meisosi in the testes of male beetles
she disocevred that during meisis 1 tehre were nine matched pairs of chromsomes (autosomes) and a pair of unequal size
she named the larger of the unmatches X chromsomes and the smaller one the Y chromsome
stevens further observed that after emisis two types of sperm were prodcued: half with nine autosmes and one x chrosmome and half with nine autosomes and one y
eggs on the other hand contaiend nine autsomes and one x chromsomes
eggs fetrlized by an x ocnating sperm developed as females while eggs fetrlized by a y containing spemr became males
stevens concluded that the x and y chrosomes dtermine sex: XX beetles are females nad XY are males
several resarachers studing otehr organisms soon verified that in many sexually reproducing species, two disticnt chrosmomes - known as sex chrosmomes - provide the basis of sex dtermination
one sex carries two copies of the same chromsomes (matched pair) and the otehr sex has one of each typeof sex chromsome (unmatched pair)
the cells of typcal females has 23 pairs of chromsomes
the two chrosomes of each pair incluidng the sex dtemrining x chromsomes appear to be idneitcial in size and shape
in males however one unmatched pair is present: larger is x and smaller is y
aside from this the two sexes arent distingusable by any other pair of chromsomes
thus genetcist can designate females as XX and males as XY and represent sexual reproduction as simple cross between XX and YY
if sex is an inhertied trait dtermined by pair of sex chromsomes that seperate into diff cells during gamete formation then anXX with XY cross oculd account for both the mutual exlcusion of sexes and the near 1:1 ratio of males to females which are hallmark features of sex detrmination
in humans the SRY gene on y chrosmome determines maleness
its the presence or absence of y chromsome rather than number of x chromsomes that decides the morpholgical sex of a human zygote; any person caryring y chromsome will have the physical charcertics of a male
this statement comes from stydy of human anueploids - ppl whse cells are msiisng a chromsome or have an extra crhsmome
ex. rare humans with two x and one y are males with abnromalties called klinefelter syndrom
males with this syndrome are tall, thin and sterile and have cog diabailties
that these idnivduals are males show that two x chromsomes are insurfiecnt for female dveelopment in presence of a y chromsome
in constarts humans carrying an x and no second chromsome (XO) are females with turner syndrome
such females are sterile, lack secondary sexual charcetrics like pubic hair etc
even thouhght they only hvae one x, they dvelop as females bc they have no y
in 90s rrsearchers disocvered that its not the entire y chrosome but rather a single y chromsome psecific gene called SRY (sex detmring region of Y) that is the primary dterminant of maleness
the evdience implacting sry came from so called sex reversal: the existence of xx males and xy females
in many males with xx sex reversal one of the two x chromsoems caries a portion of y chromsome
although in diff xx males diff portions of the y chrosmoems are found on the x, one partciualr gene, sry , is always present
females with xy sex reveasal in constast always have a y chrosmome lacking a functional sry gene; the portion of y containg sry is either replaced by portion of x or the y contains a nonfucntional mutant copy of sry
later expeirments with mice confirmed that sry indeed detrmiens maleness
approx 6 weeks fater fertlization sry proteins atcviates testes dveeloment in xy embryos
the mebryonic testes secrete hormones taht trigegr the dvelopment of male sex organs and prevent the formation of female sex organs
in the absence of sry porteins, ovaries dveelop instead of testes and other female organs dveelop by default
human x and y chromsomes also contain genes unrelated to sex
sry is one of abt 50 proetin coding genes on the human y chrosome
sry as well as trhee genes required for spermatogeneis are located in the male specific region of the Y (MSY) but no wehre else in the genome
however contarry to the name, scattered throughout msy are several egens that also exists on the x chrosmome
these genes affect the function of cells and tisseus all over the body
in fact eight of these shared genes are essential for male viability bc without the y linked copies, the single gene copies on x chrosmome doesnt supply suffifent protein
the two ends of the y chromsome are called the pseudoautosomal regions (PARs) bc nearly idnetcal dna seuqences are present at the ends of x chromsomes
the two PARs (1 and 2) togetehr contain abt 30 genes, copies of which are found on both the x and y chromsomes
the PARs allow the otehrwsie mostly dissimilar X and Y chrosmomes to pair ith each otehr during meisiss 1
the x chromsome is much large rthan the y
it contains abt 850 protein coding genes
in contarst with gene on y, most x chromme genes have nothing to do with sex; they speify proetins needed by both males and females
the fact that the x and y chrosmomes share sevral egens sugegst y evolved from x and in proces of being y the x lost almost all of its genes except those few required in two copues and those such as sry that acquired a specific function in males
transgenic mice prove that sry is maleness factor
genes similar to human sry have been didnetfied on y chrosmoems of most mamalian species
in 91’ researchers used mouse transgenic tech to show that the sry gene is crucial detrminat of maleness
a trangenic mouse is one with a chrosmome that conatins copies of a gene that came from another idnivdual of the same species, diff species or a egen synthesized in test tube
such genes are called transgenes
one focusi of genetic engrineeirng is etch for the manipulation and insertion of transgenes
indivduals or cells with transgenes are said to be trasnformed with the trasngene
to detrmine if sry is sufficent to dtemrine maleness, researchers wnated to introduce copies of the mouse sry gene into genome of chromsomally female mixe
if sry is crutcal for malenss then xx mice conatiing sry transgene would be male
first scinetsit isolated the dna of mouse sry gene using cloning tech
using a method called pronucelar injection, trangenci mcie wer egenrated that conatined sry gene on tehri autsoomes
to perform proncuelar inejction, researchers collecedt many fetlrized mouse eggs from mated females and injected the sperm or eggs ncuelus )proncuels in zygote) with hudnreds of copies of sry gene dna
enzyymes in proncuelus integrated the dna into random locations in the chrosmome
after the injected zygotes matured into ealry emrbyos they were impalnted in surrogates
when the mice were born, cells from their tails were tested for the presence of the sry transgene using molecular biolgical techniques
a transgenic mouse transmred with teh sry obtained - even though chrosmally xx, its phenotypcially male
so the sry gene alone is suffuienct to dtemrien maleness
species vary enorumsly in sex dtemrinnng mehcnaisms
other species show variations on this xx versus xy chrosmal stagey of sex detrmination
in fruit flies, although nromal females are xx and males are xy, ultimately the number of x (not presence or absnece of y) that dtermines sex
the diff repsonses of humans and fruit fleis to same unsual compelnent of sex chromsomes, reveal that the mechnaisms for sex dtermiantion differ in fleis and humans
xxy flies are famles bc two x’s, but xxy in humans are males bc of y
concversly bc they have one x the xo flies are males and xo humans are female bc tehy lack y
the xx=female and xy= male stargey of sex dtermination is by no means universal
some species have only a single kind fo sex chromsoem
in moths, famles are xx but males are xo etc
in other species inclduing birds, its the males that have matching crhosmes while females have unmatched set
the sex having two diff sex chromsoems is dtemrined the heterogameteic sex bc it gives rise to two diff types of gametes
concversly the sex with two similar sexc chromsoems is the homogametic sex
the gametes of the heteorgametci sex would contain ietehr x or y in case of male humans but gamtes of homogatmetic sex would only cnontain x
yet other species lack specilzied sex chromsomes
ex. female and male bees have same knd of chrmsomes but females are diploid while males are haploid
in fish species sex is dtemriend by temp (envrient infleunce phenotype)
