EK B2 Reproduction system and development COPY Flashcards
Mitosis
Mitosis is a clonal division (means two cells identical to parent, two daughter cells diplioid how we replicate somatic tissue most of tissue of body except for egg adn sperm cells)
Produces two diploid cells identical to the diploid parent
Used for cell replication in somatic tissues
Two mechanisms for passing down genetic information:
mitosis and meiosis
meiosis
Meiosis is a reductional division- means start with diploid get haploid
Produces four haploid gametes from a diploid parent
Takes place only in the gonad ONLY TAKES PLACE HERE
Process for producing egg and sperm cells
Fusion of haploid gametes during fertilization reconstitutes diploid zygote organism** which allows offspring to be diploid again
Cell cycle
- Cells move through a cell cycle
- Four phases of the cell cycle: G1, S, G2, M
- First three phases are “interphase”
- S phase is synthesis, when DNA replication occurs
- During G1 and G2 phases, cell growth and protein synthesis
- M phase is mitosis
- Non-dividing cells (e.g., neurons) are permanently arrested in G0 phase (before S)
- Loss of cell cycle control can lead to cancer
diploid
2n= 46 chromosomes in humans
n= 23 pairs** but if took a skin cell it would have 2 x n= 46 chromosomes two copies of chromosome 1, two copies of chromosome 2 and 2 copies of chromosome 3….
haploid
n= 23
- chromosome 23 is X in a female always, and X or Y in a male*
- NO PAIRS
pairs 1-22 chromosomes
autosomes
pair 23 chromsome
sex chromosome
female: XX
male: XY
so 23 is XX or XY
cell cycle 2
- a sliver of cell cycle is mitosis, but then the whole rest of this is interphase, everything except for Mitosis, M section*
- interphase broken up into: G1, S, G2
- G1= cell growth
- S= stands for DNA synthesis which is the same as replication* when doubling amount of dna in preparation for cell division*
- G2= another growth period
- M= actual division Mitosis
G0
- not all cells dividing all the time, some in dormant phase called G0 offramp called G0
- this is like neurons* for exampe are not actively dividng they are at rest in G0 so that is a way that they can not be actively going around and around the cell cycle
- cells can go into G0 for a little while and then go back out again, but neurons are permanetly in G0
- they are considered postmitotic cell not going around cell cycle and dividing, why neuron damage is os bad no cell cycle to create new cells easily
- not all cells divide with same frequency= NEURONS DO NOT DIVIDE* but then have cells that get a ot of wear and tear adn dividing a lot liek skin cels dividing all the time, lining of our GI tract food passing through those cells divide a lot so epithelial linings internal or external on surface of body tend ot be rapidly dividing or consistently dividing*
who does cell cycle the most
- skin cells, GI inner cells/lining of GI tract
- BUT THE MOST IS CANCER** this the key underpining for why they are so deadly
- very rapidly dividing but unregulated BAD* cell division not normal its bad*
- neurons- non dividing
centrioles, centrosomes and mitoic spindle
Each cell has a centrosome
Centrosome duplicates in S phase (now two)
In mitosis, the centrosomes organize microtubules and the spindle
Kinetochore microtubules attach to kinetochores of chromosomes
Polar microtubules overlap with each other (do not attach to kinetochores)
Aster microtubules help support spindle
homologous chromosomes vs. sister chromatid
Homologous chromosomes are non-identical maternal and paternal copies of a pair
Sister chromatids are identical chromosome copies from DNA replication
Sister chromatids are linked at their centromere
mitosis card 2
5 phases of mitosis
• Interphase: DNA has already replicated, but chromatin is decondensed
• Prophase: nucleus breaks down, chromosomes condense
• Metaphase: chromosomes align on metaphase plate
• Anaphase: sister chromatids separate and are pulled towards poles
• Telophase: chromosomes decondense, cytokinesis divides cytoplasm to daughter cells
Motor proteins are critical for chromosome separation
Kinetochore microtubules lose tubulin subunits, pulling chromosomes to poles
Polar microtubules push against each other, pushing the spindle ends apart
metaphase
- chromosomes align on metaphase plate
- chromosomes line up single file on metaphsae plate, 2n=4
- get daughter cells when pulled apart with 4 each, 2n each* and it will have all the same alleles so genetically identical to original diploid cell that entered into mitosis
sister chromatids
- daughter cells right at end of mitosis do not have same amoutn of dna as parent cell in metaphase
- sister chromatids are two lines together, genetically identifcal to each other all the same alleles*
- in mitosis sister chromatids separate, anaphase they pull apart, what separates during anaphase its the sister chromatids*
- if look at daughter cells in order for them to undergo mitosis again and make 2 daugher cells of its own has to go around cell cycle, duurign S phase whole deal with replication is go from one chromosome to sister chromatids, so replication doubles the amount of DNA but does not change the numebr of chromosoems***
- BOTH 1 CHROMOSOME, middle point on chromosome called centromere** so formal way of saying this to count numebr of chromosomes ocunt numebr of centromeres**** if think abotu X like picture with sister chromatids one centromere, one belly button, not total amount of DNA number of centromeres that defines number of chromosoems*
centrosomes
those are microtubule organizing centers for the cell*
questions on mcat- think about centrosome, these spindles made of microtubules, microtubule organziing centers are centrosome, command center for microtubules spindles that have to attach to centromeres of each of these chromosomes
if cell needs to organize microtubules for some other purpose, cell can also make use of centrosome, which part of the cell is in charge of organzing other microtubules for some othe rprocess they tell you about, if process governing where cells beign set up that is the centrosome* even if not talkign about mitosis some other thing cel using microtubules for*
centrioles 1
- centrioles help centrosomes do their job
- animals do have centrioles* centrosomes contain centrioles
- centrosome is organizing microtubules**
centromere
each chromosome has 1 centromere the belly button, how we count dna**
like glycolysis, etc names words sound the same and come up in mc questions
Interphase:
Interphase: DNA has already replicated, but chromatin is decondensed
Prophase:
Prophase: nucleus breaks down, chromosomes condense
Anaphase
Anaphase: sister chromatids separate and are pulled towards poles
meiosis part 1
Meiosis is a reductional division
One diploid cell → two cell divisions → four haploid gametes
DNA replication before meiosis I
Prophase I: nucleus breaks down, chromosomes condense
Homologous chromosomes synapse (form synaptonemal complex)
Recombination (crossing over) occurs
Metaphase I: tetrads line up on metaphase plate, held together by crossovers
Anaphase I: crossovers are resolved, homologous chromosomes separate
Telophase I: daughter cells form and cytokinesis takes place
• Sister chromatids are still joined
prophase 1
meiosis
nucleus breaks down, chromosomes condense
Homologous chromosomes synapse (form synaptonemal complex)
Recombination (crossing over) occurs
where you get crossing over*** the mechanism for getting recombination in gametes the time when that is occuring is prophase 1*
if cell is 2n, total of 4 chromosomes, in mitosis ignore fat chromosomes exist as pairs, now pairs find each other; say these are the two copies of chromosome 1, same genes but not necessarily same alleles, when crossing over occurs allele for blue eyes swapping over with allele for brown eyes* still gene for eye what defines pairs, genes for eye color here is the gene for ear wax etc
tetrad
- what is important in Prophase 1= still total 4 chromosomes, pair members are finding eachother and form a temporary unit called tetrad to enable crossing over
- tetrad= homologous chromosomes come together
- these are the two copies of pair number 1 and two copies of pair number 2 find each other
- 4 total chromosomes, before tetrads were formed
Metaphase I (meiosis I)
Metaphase I: tetrads line up on metaphase plate, held together by crossovers
DO NOT LINE UP SINGLE FILE, homologous pairs line up together*
Anaphase I meiosis I
Anaphase I: crossovers are resolved, homologous chromosomes separate
PAIRS SEPARATE*
get 2 haploid daugher cells, already genetically different than parent cell becuase parent cell was diploid*
Telophase I meiosis I
-daughter cells form and cytokinesis takes place
• Sister chromatids are still joined
this is in meiosis I*
meiosis II
easy just like mitosis*
n daughters have half amount of dna because sister chromatid have separated but same number of chromosomes*
Prophase II: nucleus breaks down, chromosomes condense
Metaphase II: chromosomes line up on metaphase plate
Anaphase II: sister chromatids separate
Telophase II: nuclei reform, cytokinesis proceeds
• Products are four haploid cells (with recombined chromosomes)
Prophase II
Prophase II: nucleus breaks down, chromosomes condense
non-disjunction
- abnormal separation* problems with separation**
- can occur in meiosis I or in meiosis II, question asked before which is more serious? which leads to more abnormal gametes*
- not always sticking together forever, but for too long so when meiosis is finished those two ended up on one side and then the other pair separated normally*
- can get ultimately n+1, n-1 n-1, n+1
- EARLIER in meiosis I is more serious, effects closer to trunk of tree all branches get effected!!
- when nondisjunction happens in meiosis II only effects half progeny daughter cells*
Metaphase II
Metaphase II: chromosomes line up on metaphase plate
Anaphase II
Anaphase II: sister chromatids separate
Telophase II
Telophase II: nuclei reform, cytokinesis proceeds
• Products are four haploid cells (with recombined chromosomes)
meiotic defects and nondisjunction 2
In non-disjunction, errors occur in chromosome segregation
Failure of chromosome separation in meiosis I or II yields abnormal gametes
One gamete lacks chromosome, other has extra chromosome
Results in trisomy or monosomy after fertilization
Almost all trisomies and monosomies are lethal
Down’s = trisomy 21
Kleinfelter’s = XXY
Turner’s = XO
image nondisjunction in meiosis I
image of nondisjunction in meiosis II
trisomy and monosomy
normal fertilization=n (egg) + n (sperm) –> 2n zygote
abnormal case: n+1 (eggs) + n (sperm) –> 2n + 1 is called trisomy, one pair has an extra chromosome
n-1 (egg) + n (sperm)–> 2n-1 monosomy
any abnormal cases when do not get n for zygote, are trisomy and monosomy***
you can have trisomy or monosomy in an egg and sperm! so sperm can also have n+1
aneuploidy
any abnormal cases when do not get n for zygote, are trisomy and monosomy***
vast majority of these pregancies do not survive** reflects something seriously wrong with embryo**
some trisomies and monosomies that are actually less serious
-if you have a trisomy of chromosome 1 not physically possible to walk this earth, can get trisomoy with chromosome 21 which is down syndrome, not liek chormosome 1 undergoes nondisjunction more than any other chromosome its actually a milder phenotype can survive with trisomy 21 why have that condition, nothing special about chromosome 21 that makes it stick to iteslf more it just can survive*
sex chromosomes disjunction/ trisomy
Kleinfelter’s = XXY- very mild, a lot of ppl with that do not know they have it, can cause problems with fertility* but up until that poitn can look like a male never known*
Turner’s = XO- turner’s present as female, not deadly causes problems with fertility or cardiac issues but definitely something that ppl live with*
can have trisomy/monosomy at sex chromosomes and survive; normally someone who has Y chromosome have male phenotype
Down’s
= trisomy 21
reproductive system
- Fusion of haploid gametes → fertilization
- In humans, fertilization occurs internally
male anatomy
sperm cells created in testis, meiosis in there
- epididymis immature sperm cells mature, in men the sperm cells mature and gain their tails allowing them to swim, but maturation process happens in epididymis
- so they are stored and mature in epididymis
- during ejactulation, sperm cells go up around called vas defens
- if you following up and around, then tube goes down and out urethra* same as in men, same tube carries sperm and urine*
know on image vas deferens, testis, epididymis so vas deferens then to urethra and out*
3 accessory glands in male anatomy-
know seminal vesicle, prostate gland, bulbourethral gland
3 accessory glands in male anatomy 2
Seminal vesicles add fructose and prostaglandins
Prostate gland adds alkaline secretion
Bulbourethral gland adds mucus lubricant
know along the way as sperm is traveling up around through vas deferens, three glands that add secretions! 3 accessory glands add secretions to sperm so sperm cells plus secretions make semen
spermatogenesis 1
meiosis starts at primary spermatocyte
after meiosis I have 2 secondary spermatocytes, after meiosis II you have 4 spermatids* those mature into 4 spermatoza (sperm cells) the mature sperm cells*
Sperm are generated throughout adulthood
Spermatogonium → 1° spermatocyte → two 2° spermatocytes → 4 spermatids → 4 spermatozoa
occurs inside seminiferous tubules* other cells called sertoli cells which are also present and support cells, shown ind iagram in purple, if looking inside of seminiferous tubule inside testy see cells in different stages of meiosis doing there thing, so see primary and secondary then also these sertoli cells providing additional support
sertoli cells
Sertoli cells nurse developing spermatids
Spermatids mature into spermatozoa with tails
structure of sperm cell
- sperm tail flagella made of micotrubules, n in picture where nucleus and DNA are
- brownish part area called midpiece where there is a ton of mitochondria, again because sperm cells need to swim so need to be able to make lots of atp
- Sperm has head, midpiece, and flagellum tail
- Head contains sperm nucleus
- Midpiece contains coiled mitochondria
- Flagellum is composed of 9+2 microtubule structure
- Acrosome at sperm tip has enzymes for egg penetration=acrosome enzymes for penetrating egg at top of sperm cell
male sexual hormones
GnRH secretion from hypothalamus begins prior to puberty, continues in adult
GnRH → stimulates anterior pituitary → FSH and LH
FSH → stimulates Sertoli cells and spermatogenesis
LH → stimulates interstitial (Leydig) cells → produce testosterone
Testosterone is the main androgen
Testosterone needed for spermatogenesis
Testosterone needed for secondary sex characteristics (bone, muscle, hair, voice)
Testosterone deprivation → sterility
Negative feedback loop: testosterone inhibits GnRH and LH secretion
female sex anatomy
Female gonads are the ovaries, gametes are eggs (ova)
Ova are released into oviduct (fallopian tube)
Fertilization of egg occurs in oviduct
Blastocyst implants in uterus wall
Uterus epithelium = endometrium (lining of the uterus)
If no fertilization, endometrium is sloughed off = menstruation
Vagina → cervix → uterus
bottom of uterus is cervix* fertilizaton occurs sperm has to swim all the way up through vagina, through uterus and then fertilization occurs in oviduct
spermatogenesis 2
Spermatogonium → 1° spermatocyte → two 2° spermatocytes → 4 spermatids → 4 spermatozoa
Spermatogonium is diploid progenitor cell
Spermatogonium differentiates into primary spermatocye
Primary spermatocyte is diploid and enters meiosis
Meiosis I produces two secondary spermatocytes
Meiosis II produces two haploid spermatids from each secondary spermatocyte
Primary spermatocyte → four spermatids
Sertoli cells nurse developing spermatids
Spermatids mature into spermatozoa with tails
Maturation occurs in epididymis
During maturation sperm loses most cytoplasm
LH
stimulates production of testosterone, obviously if testosterone is high does negative feedback on brain on hypothalamus and anterior pitutitary
LH → stimulates interstitial (Leydig) cells → produce testosterone
receptor on testes
FSH
stimulates spermatogenesis*
FSH → stimulates Sertoli cells and spermatogenesis, hormone that mostly aggressively binds to testes and do spermatogenesis, there are receptors for FSH and LH on the testes those are both protein hormones** testosteorne is a steroid*
testosterone
- main androgen= which is a category of steroid hormones* think about testosterone and androgen being basically synonyms for purpose of mcat, obviously hormones really really similar to testosterone with small chemical modifications form family of androgens
- Testosterone needed for spermatogenesis, need it to do the spermatogenesis*
- Testosterone needed for secondary sex characteristics (bone, muscle, hair, voice) all changes that happen in puberty
- Testosterone deprivation → sterility
- Negative feedback loop: testosterone inhibits GnRH and LH secretion
GnRH
GnRH secretion from hypothalamus begins prior to puberty, continues in adult
GnRH → stimulates anterior pituitary → FSH and LH
hypothalamus uses different hormones to signal to anterior pitutiary** so its just the thing secreted by hypothamalus to atnterior pitutiary
Gn releasing hormone, telling anterior pituitary to release FSH and LH
male hormone feedback loop
fertilization progress
Vagina → cervix → uterus
if fertilizaiton occurs embryo will implant in lining of uterus* fertilization in oviduct if fertilizatin occurs most of the time it doesnt occur, but if it does it happens in the oviduct, 5-6 days later have an early embyro that would implant in wall of uterus in endometrium linng
from a medical point of view embryo implanting in endometrium lining from religious points of view it all begins at fertilizaton= big difference if you have a form, intervention that prevents implantation* from a medical point of view most doctors would call that birth control but some catholic people would call that a form of abortion interfering with life after life has begun* if it all begins when fertilization occurs then everything after that is absorption, but from a medical poitn of view pregnancy begins at implantation*
oogensis 1
- primary oocyte then after meiosis I and onset of meiosis II secondary oocyte, uneven division of cytoplasm in women, in meiosis instead of getting two haploid cells the same as eachother we get these two daughter cells one full fledged cell secondary oocyte, other one doesnt have much cytoplasm called first polar body degenerates and pulls alway, cytoplasm being horded to one side**
- same thing happens again in meiosis II ther eis an ovum and a second polar body that forms, a repository for extra dna*
- adaptive for us because cytoplasm contains lots of proteins, nutrients, embryo will get all of it smitochondria then from ovum* all cytoplasm, ribosomes proteins why mitochondrial dna passed form mother** becuase cytoplasm and mitochondira coming from ovum*** and sperm is mainly contributing dna*
difference btw men and women (oogenesis)
- one big differnce uneven divisin of cytoplasm during meiosis in females, second big difference is timing of everything**
- we make primary oocytes in utero , suspended during beginning of prophase 1 of meiosis when we are born* different from men men generate primary spermaties from puberty on
- we do not keep making primary oocytes we are born with a lot of the, but do not make any more later*
- primary oocytes when we ar eborn are just starting meiosis I but suspended in prophase of meiosis 1 and stay there until we hit puberty once hit puberty finish meosis I, cell type we are releasing when we ovulate is a secondary oocyte***
- matured 1 at a time** so what they are doing then in the ovaries is completing meiosis I and entering into meiosis II we do not do the rest of meiosis unless a sperm cell makes contact with a secondary oocytes*** so most of the time in our lives we do not go through the rest of meosis *
- if sperm cell enters secondary oocyte cell relaly quicjly finishes meiosis II becomes an ovum, which doesnt stick around very long because sperm cells on its way and then as soon as nuceli fuse we have a zygote the first cell of the embryo
oogenesis 2
Oogonium → 1° oocyte → polar body + 2° oocyte → ovum
Before birth, oogonia differentiate into primary oocytes
Primary oocytes pause in prophase I of meiosis until puberty
At puberty, monthly hormonal cycle regulates ovulation
FSH → follicle matures, primary oocyte finishes meiosis I
Primary oocyte → polar body and a secondary oocyte
Meiosis II in polar body → two polar bodies (but not in humans, stops at polar body)
Meiosis II in secondary oocyte (paused until fertilization) → large egg, small polar body
egg and follice structure
Ovum (egg) + support cells = follicle
Egg is surrounded by extracellular matrix = zona pellucida
Zona pellucida is surrounded by follicular granulosa cells = corona radiata
Ovulation ejects ovum into oviduct
Follicle portion that remains in ovary is the corpus luteum
Egg is much larger than sperm
Egg contributes cytoplasm and mitochondria to zygote
follice
Ovum (egg) + support cells = follicle
Egg is surrounded by extracellular matrix =
zona pellucida
menstrual cycle 1
- hypothalamus releases GnRh
- tells anterior pitutiary to release FSH and LH, FSH is called follicle stimulating hormone, together with LH sitmulates follice to grow within ovaries, within ovaries we have little follicles where oocytes undergo meiosis*
- follice growing (ovary and follice developing gametes have meiosis going on, but also secreting hormones so ovaries are also endocrine gland)
- estradiol secreted by growing follice in increasing amounts, same thing as estrogen
- feedback loop- look up at hypothalamus initially negative feedback, red arrow to anterior pitutiary, inhibited by lwo levels of estradiol; the main thing to focus on is at beginning low levels estradiol putting breaks on brain, green arrow on hypothalamus once estradiol gets above certain concentrations DOES POSITIVE FEEDBACK* on brain in which higher estrogen means more GnRH, more FSH and LH stimualte follice even more means more estrogen means more stimulation of ovary* so there is a building effect that occurs*- can see how estradiol starts to peak because of positive feedback, goin gup and up brain really stimulating ovaries a lot, get a lot of estrogen, that causes number 6
menstraul cycle 2
- LH surge causes ovulation very important half way through cycle*
- maturing follice
- corpus lutuem, now hormone pumping machine here, continues to pump out estrogen or estradiol, but also now crankign up progesterone*
- when progesterion and estrogen (estradiol) together that really causes the build up of endometrium lining, gestation growth of embryo so really really promoting conditions necessary if a pregnancy were going to occur* -the combination of estrogen and progesterone do negative feedback on hypoathalums, red arrow going to hypothalamus, *if estrogen alone does positive feedback but as soon as you have the ocmbination of estrogen and progesterone it does negative feedback**which is what you want at this stage, ovulation has occured oocyte has left ovary up in ovidcut maybe fertilized maybe not but wouldnt make sense to start maturing another follice at this point, having negative feedback on the brain at this point is good, do nto want FSH adn LH to stimulate a need egg to develop at this point*
THEN corpus leuteum starts to degenreate, that just happens after a certain amount of time, corpus luteum temporary structure not built to last, after about 2 weeks it starts to break down* corpus leutum was producing estrogen and progesterone so as it breaks down get less o those* which means less stimulation of endrometrial lining which means at a certain point if sluffs off and we get our periods
follicular phase and luteal phase
when follic growing–> estradiol secreted by growing follice in inc amounts
luteal phase- progesterone and estroadiol secreted by corpus luetum, pumping out hormones!
menstrual flow phase
- day one line sheds
- as soon as endometrial lining starts going off we are technically back to the beginning, cycle starting over if you do not have progesterone or estrogen cycle begins again with brain also
- hypothalamus releases more GnRH back to number 1, anteiror pitutiary releases FSH and LH go to ovary and start again with new follice maturing
Zona pellucida is surrounded by follicular granulosa cells =
corona radiata
fertilization
releases oocyte into oviduct, if fertilized by sperm then a zygote is formed and then that zygote starts doing a whole bunch of mitosis, 1 cell to 2 cells to 4 cells to 8 cells while moving toward uterus, then if it implants itself in endometrial lining of uterus a pregnancy begins*
During ovulation, secondary oocyte is ejected into oviduct
Oviduct cilia sweep oocyte towards uterus
Fertilization by sperm occurs in oviduct
Only one sperm can fertilize an egg
Upon fertilization, secondary oocyte completes meiosis II
Sperm and egg pronuclei fuse
Early development begins
Early embryo (blastocyst) implants in uterine wall
ectopic preganacy
- Implantation in oviduct = ectopic pregnancy
- if embryo starts growing and getting bigger and bigger, not meant to incubate a larger embryo or fetus so at a certain point first of all the women will start to be in massive pain embryo will start pushing out on walls of fallopian tube, if tube ruptures life threatening situation
- implanatation occurs in oviduct, fertilzied egg and embryo supposed ot move through fallopian tube and implant in uterus, if for some reason that early embryo gets stuck in fallopian tube and keeps growing there women has to have falliopian tube surgeically removed at that point ex. whitney port/arielle charnas
endometriosis
- risk factor for that is endometriosis, underdiagnosed condition women who have really bad periods or a lot of pain around period have extra growth of tissue** means endometrial lining =those cells start growing in the wrong places including fallopian tubes
- very painful can be mild or not but that is a huge risk factor for ectopic pregancy all of that is really
- once there is this tissue growing all over the place, if not painful enough to warrent surgery very hard to diagnose; endometrial tissue starts growing all over the place, can cause other parts of abdominal cavity to stick together in extreme cases can have all this stuff sticking together*
female hormone cycle and ovulation 1
Ovulation every ~28 days, from puberty until menopause
GnRH is released from hypothalamus → anterior pituitary → FSH, LH
FSH, LH trigger follicle maturation
Follicle begins to secrete estrogen → inhibits secretion of GnRH, FSH, LH
Later, accumulating estrogen at higher levels → surge in LH, FSH
LH surge causes ovulation
After ovulation, corpus luteum remains
female hormones and ovulation 2
Corpus luteum secretes progesterone and estrogen for about 2 weeks
Progesterone stimulates endometrium thickening to prepare for pregnancy
Progesterone/estrogen → inhibit secretion of FSH, LH
If no fertilization, corpus luteum degenerates → loss of progesterone/estrogen
Endometrium is sloughed off = menstruation
Inhibition of LH and FSH is relieved
GnRH begins to increase, cycle repeats
twins dizygotic
- two separate eggs fertilized
Two eggs can be released and fertilized by separate sperm = dizygotic twins
Dizygotic twins are genetically different, can be different sexes
- di zygotes= means two diff zygotes
Monozygotic twins
- one sperm cell fertilizing one oocyte, and then early embryo divides* then get identical or monozygotic twins; fertilization occurs and you have the zygote
- all from same zygote all same dna identical
- If a fertilized two-cell zygote splits, two embryos result = monozygotic twins
Monozygotic twins are genetically identical*
totipotent
means anyone of these cells can become anything!
when ppl talk about embryonic stem cells, can become any part of embryo or whole embryo, talking about cells up through this 8 cell stage
if for some reason at 2,4, 8 cell phase gets separated from group develops on its own genetically identical generated through mitosis all same exact dna, but look different= identical twins
what is a zygote
= fertilized egg, haploid nuc from egg and haploid from sperm come together get ferilized cell called zygote*
pregnancy 1
if emrbyonic implanation its the blastula*, at this point its very important to sustain endometrial lining, blastua will not last long if woman gets her period, problem is corpus luteum is degenerating at this point* not built to last*
what happens when embryo present embryo secretes hormone called hCG which then tells corpus luetum not to degenerate and keep producing estrogen and progesterone* ; corpus leutum keeps pumping out progesterone and estrogen, first trimester estrogen and progeserone sustaining endometrial lining is all coming from corpus luteum* by the end of the first trimester things have developed enough with pregnancy that the placenta (cells contribtued by fetus and cells contributed by mother) endocrine gland source of estrogen and progesterone for the rest of the pregnancy*
on pregnancy test they are looking for hCG*
pregnancy 2
Estrogen and progesterone are needed to maintain pregnancy
Progesterone/estrogen secreted from the corpus luteum, and later, the placenta
Human chorionic gonadotropin (hCG) secreted by fertilized embryo
hCG maintains corpus luteum until placenta forms
No mixing of maternal and fetal blood
~38 weeks gestation
Oxytocin induces uterine contraction and labor
placenta
Placenta is interface between mother and fetus
Placenta transports nutrients to fetus and removes wastes, very important to regulate what passes across placenta like oxygen and nutrients, carbon dioxide and waste in the other direction, antibodies that can cross the placenta, if mother is a smoker nicotine will cross placenta* how material is passed from mother to fetus during a pregnancy
early embryonic development
Early mitotic divisions of zygote are rapid = cleavage
During cleavage, cell number increases but embryo size is constant
1 → 2 → 4 → 8 → 16 → 32 → 64…
32 cell embryo ball = morula
64 cell embryo onwards = blastula
Blastula/blastocyst has fluid filled interior cavity, outer trophoblast, inner cell mass
Outer trophoblast → gives rise to placenta
Inner cell mass → gives rise to embryo
Blastocyst enlarges → becomes gastrula
Gastrula undergoes gastrulation (movement and infolding of tissue layers)
Cells migrate inwards, away from the surface of the gastrula
Infolding of tissue gives rise to the three primary germ layers
primary germ layers
Ectoderm = epidermis, mouth, nervous system, lens of eye
Mesoderm = bone, muscle, blood, heart, kidney, dermis, hypodermis, connective tissue
Endoderm = lining of GI tract, liver, pancreas, lungs
Ectoderm =
Ectoderm = epidermis, mouth, nervous system, lens of eye
Mesoderm =
Mesoderm = bone, muscle, blood, heart, kidney, dermis, hypodermis, connective tissue
Endoderm =
Endoderm = lining of GI tract, liver, pancreas, lungs
where do brain and spine come from
blue ectoderm, red mesoderm, yellow endoderm
see here mesoderm has structure called notochord made of mesoderm, red notochord induces hte overlining ectoderm to become the neural tube and then that develops into the brain and spinal cord, that process is called neurlation** how there is a neural plate folds up into neural tube, notochord structure causes formation of neural tube which then becomes brain and spinal cord
so notocord does not become the spinal cord IT INDUCES** THE NEIGHBORING CELLS TO BECOME A NEURAL TUBE WHICH THEN BECOMES SPINAL CORD
notochord degenerates*
spinal cord and brain made from ectoderm*
determination
cell commited to a particular develomental pathway
differentation
certain point fate is determined but then differentiates which is the follow through; fate can be determined early, but differentiation may be apparent only late
Differentiation = specialization in function of cells or tissue is apparent
Pluripotent =
= fate is partly determined, can contribute to many but not all tissues
only have certain range, limited set of cells
differentiation and determination
Fate of a cell can be determined early, but differentiation may be apparent only later
Cells of very early embryo are totipotent
Totipotent = can contribute to all tissues
Identical twins reflect totipotency of early zygote
Pluripotent = fate is partly determined, can contribute to many but not all tissues
As development proceeds, fate of cells becomes progressively more determined
gene expression and differentation
All genes are present in every cell
But not every gene is transcribed in every cell
Differential gene expression drives differentiation and development
A gene can be expressed constitutively = on in all tissues
A gene can be expressed tissue-specifically = on in select tissues
Expressing subsets of genes differentiates tissues and allows specialization
In brain, a certain combination of genes, say, A, B, C, D are on
In liver, a different combination of genes, say, B, E, F, G are on
In kidney, a different combination of genes, say, A, D, G are on
Transcription factors control gene expression patterns during development
cell communication during development
Cells communicate and signal to each other during development (long range secreted proteins, short range neurlation)
Signals can alter cell fate or gene expression
Induction of neural plate by notochord is an example of signaling
Communication can be direct, short-range
Transmembrane ligand on one cell binds to receptor on another cell
Communication can be long-range, involving secreted proteins
4 main tissue types
Epithelial = cell sheets that cover external and internal linings (resp, digest, excr, repro)
Nervous = brain, sensory structures
Muscle = smooth, skeletal, cardiac
Connective = bone, cartilage, blood, fat, remember blood is defined as special connective tissue**
epithelial tissue
Epithelial tissue can be simple, with one layer (e.g., alveoli)
Epithelial tissue can be stratified, with multiple layers (skin)
Endothelial tissue lines vasculature and is similar to epithelium, which make up lining of blood vessels** capillaries are one cell thick, shape of cells for endotheliam are very similar to epitheliam skin cells same shape
enodthelial are wlals of capillaries or blood vessel linings, wrap it with other cell layers adn smooth muscle, still part touching blood itself is the endothelial cell layer
SO SIMILAR BUT DIFFERENT*
The main difference between epithelial and endothelial cells is that epithelial cells line both internal surfaces and external surfaces of the body whereas endothelial cells line the internal surfaces of the components of the circulatory system.
Endothelium generally lines fully internal pathways (such as the vascular system), while epithelium generally lines pathways that are open to the external environment (such as the respiratory and digestive systems).
apoptosis
Some cells are programmed to commit suicide = apoptosis
Apoptosis is necessary for development
Example: webbed limb buds give rise to hands with distinct fingers
connective tissue
Composed of cells and an extracellular matrix with protein fibers
Main protein fiber is collagen
Basic connective tissue can be loose or dense
Loose connective tissue: less fiber, more cells (e.g., submucosa layer covering GI tract), what packs around organs*
Loose connective tissue surrounds many organs and structures
Dense connective tissue: more fiber, fewer cells (e.g., tendons and ligaments)* when say more fiber they mean protein
Specialized connective tissues: bone, blood, cartilage, fat
loose connective tissue
Loose connective tissue: less fiber, more cells (e.g., submucosa layer covering GI tract), what packs around organs*
Loose connective tissue surrounds many organs and structures
Dense connective tissue
Dense connective tissue: more fiber, fewer cells (e.g., tendons and ligaments)
body cavity
- Coelom = body cavity
- In humans, the thoracic and abdominal cavities are parts of the coelom
- Most bilateral animals (including vertebrates) are coelomates meaning we have a body cavity*
Parthenogenesis
= “virgin birth” with no fertilization needed = asexual, development of an egg without fertilization
Isogamy =
= gametes are morphologically similar
when you have sexually reproducing organisms, sometimes the two gametes are really similar to eachother, find that in much simpler organisms; sometimes gametes act very differnt like egg cell vs sperm cell, which is smaller and motile, in more complex animals where gametes look different called anisogomy and two similar organisms haploid fuse to diploid but very very hard to tell apart from eachother those are isogamy organisms
Anisogamy =
= gametes look different (e.g., humans)
Hermaphroditism =
= has both male and female gonads, can sometimes self-fertilize
Pseudohermaphroditism =
= intersex.
Can be genetically one sex but have some characteristics of other sex. (e.g., XY, but female sex organs and female appearance). May results from an insensitivity to sex hormones such as androgen
if issue with receptors and insensitive to testerone can be phenotypically
motor proteins in mitosis
Motor proteins are critical for chromosome separation
Kinetochore microtubules lose tubulin subunits, pulling chromosomes to poles
Polar microtubules push against each other, pushing the spindle ends apart
Telophase for mitosis
• Telophase: chromosomes decondense, cytokinesis divides cytoplasm to daughter cells
male reproductive anatomy 2
Male gonads are the testes, gametes are sperm
Scrotum contains testes and maintains cooler temperature (~3°C) for spermatogenesis
Within testes, sperm is produced in the seminiferous tubules
Sperm from seminiferous tubules enters epididymis
From epididymis, sperm enters vas deferens
Vas deferens connects to urethra
Three accessory glands add secretions to sperm, yielding semen
Vas deferens merges into the urethra
Urethra releases semen (and urine) from penis
Upon arousal, blood flow to penis yields erection
hCG
Human chorionic gonadotropin (hCG) secreted by fertilized embryo
hCG maintains corpus luteum until placenta forms
blastula
64 cell embryo onwards = blastula
Blastula/blastocyst has fluid filled interior cavity, outer trophoblast, inner cell mass
morula
32 cell embryo ball = morula
Outer trophoblast →
Outer trophoblast → gives rise to placenta
Inner cell mass →
Inner cell mass → gives rise to embryo
Blastocyst enlarges →
Blastocyst enlarges → becomes gastrula
Gastrula undergoes gastrulation (movement and infolding of tissue layers)
Cells migrate inwards, away from the surface of the gastrula
Infolding of tissue gives rise to the three primary germ layers
neurulation
Neurulation is formation of nervous system
Nervous system formed from ectoderm layer
Notochord is mesodermal rod that lies underneath ectoderm
Signals from notochord cause ectoderm to form neural plate
Process of notochord signaling = induction
Neural plate folds inward to yield the neural tube
Hollow neural tube is future spinal cord and brain
induction
Process of notochord signaling = induction
part of neurulation
cell cycle 3
spends most of its time in interphase!!! then mitosis in red where doing a bit of cell divison, goal of mitosis is to essentially create an identical cell to whatever you started with, create no differences, cells doing this owuld be somatic cells, so all nonsex cells** everything but gametes will be doing this
sex cells are doing meosis
interphase can be subdivided into 3 phases: G1, 2, G2
G1= called gap 1 when sicnetisrts looking at cells under microscope, oh nothing is happening here there is a gap taking place why called G1- what happens cell undergoing cell growth and doing normal cell activity, meanign it will be creating organelles needed to maintain energy within the cell, will be doign some protein production all while increasing their size* some cells can enter into an additional phase form G1 adn that is what is called the Gnot nondividing cells** not actually going throguh cell cycle
nondividing cells in G0
neurons, heart muscle cells, cant do anything if damage heart muscle cells some can diide but anythign damage cannot replace or fix
most cels going into next phase called S phase* in case of S phase referred to in syhtesis
s phase
and
G2
dna replication! synthesis phase, we alreayd talked abotu dna replication here is where it will take place!
G2 more growth and prepping for mitosis, checkign to see do you have enough organelles or cytoplasm for cells about to form, all these checks to make sure you have everything before split mitosis
homologous chromosomes
same genes, same order, possible different versions (alleles) of those genes
regulation
- going from G1 into S phase very very heavily regulated, want ot amke sure no mutations because after pass through into S phase we will replicate whatever we have in the cell, it is very very heavily regulated, we said that polymerase will also make some errors, errors can get intrdouced during dna polymerase replication process
- some regulation going from G2 to mitosis but not as much, already have some additonal information from replication need to get rid of not really that error prone, but morelikely mutations will occur from g1 to s
end product of mitosis
no mutations should be introduced
two daughter cells that are IDENTICAL to each other and IDENTICAL to the parent cell
I Pee on the MAT
what is cancer?
- mutations in DNA
- start from a single cell with mutations
- go through cell cycle rapidly and out of control
- spread to other tissues (metastasize)
ex. some cells in breast tissue, mutation in DNA start going through cel cycle very rapidly and out of control, grow tumor some get dislodged go into blood stream or lymph vessel you have; once in paritcular vessels can then go to other parts of body implant somewhere else, can rapidly go through cell cycle, can then go through rapidly cell cycle; lots of time remove neraby lymph nodes because if some cancer cells become dislodged and make it into vessel will go firt to lymph nodes why remove to prevent spread of it*
two kinds of cancer genes
- oncogenes
- tumor suppressor genes
proto-oncogenes
genes normally present in cell need to be coding for proteins that regulate hte cell cycle, times in our life where we want the cell cycle going don’t need to b constantly pumping out more and more skin cells because we just do not need it
we want cell cycle to be on when: ex injury, nik in skin want cells to close it, childhood growth, also before birth fetal development want cell cycle turned on, as can imagine start form one cell divide those cels over and over again until create fetus, all times want cell cycle turned on, those proteins come from protooncogenes makes sure we turn on the cell cycle to go through it and produce new cells to make sure heal the skin and can grow, most of hte times those proteins will tell cells hey do not proced throguh cell cycle, please turn this off, but in case of cancer, those proto-oncogenes get mutated to form oncogene, an oncogene which turns cell cycle permantely on it will always be active!
when tell cells to not be going through mitosis or division, oncogenes says yes please go throguh! produce more skin cells prouce more more when this shouldnt be taking place! so this is permanently ctive cell cycle how you can get tumors to form, have all these cells constantly dividing when they should not be!
tumor supprssor genes
code for porteins that stop the cell ccycle***
so what these do is monitor geneome and see if any mutatiosn take place, if happen in G 1 phase of cell cycle activate repair mechanisms to fix dna to proceed through cell cycle, if you activate these repaired mechanisms and still unable to repair dna these repressor genes will trigger apoptosis, cell death
mugh better to have one cell die off becuase neighboring cells will fill in gap better to kill it than pass on mtuation
can imagine if you do not have a tumor supporessor gene not wokring can’t stop cell cycle adn pause and repair dna, are also not going to be able to trigger apoptosis if it results, so normal cells usually repaired or killed off becuas emutated do not have that protein doing that naymroe
why have P53- halts cell cycle form going to g1 to S phase makes sure to activate repair mechansims and trigger apoptosis if too mutated which means if dont have that going staright on from G1 to S phase with that mutation****
tumor suppresor genes 2
- Code for proteins that: stop cell cycle
- Monitor genome of cells in the cell cycle
- If DNA damaged, initiate repair mechanisms
- If not repairable, then the tumor suppressor proteins trigger apoptosis
if notice dna good give it green light to go to S phase, if notice dna has become dmaged will activate repair mechansims if can sucessfuly reapir dna get green light and proceed through cell cycle
i fnot reapir mutations too great than TS proteins will trigger apoptosis WAY better to kill cell than pass it on!!! cancer literally cell division taht can spread metastaize to other tissues**
cancer summary
cancer uncontrollable cell division taht can spread metastaize to other tissues**
oncogenes- “gain of function” mutation
“stepping on the gas pedal”
tumor suppressor genes: “loss of function” mutation
“cutting the brakes” just continue on through not going to stop the car
Q2 the hormones most directly associated with testosterone production in males and ovulation in females are:
LH for both
in males, LH responsible for tesosteron reproduction and FSH is responsible for spermatogenesis** aka sperm productioj
no testosterone spermatogenesis will not proceed normally,
Q11 Which of the following is NOT a difference btw meiosis I and meiosis II?
A. there is crossing over in meiosis I but not in meiosis II
B. centromeres divide in meiosis II but not in meiosis I
C. homologous chromosomes separate in meiosis I but not in meiosis II
D. For each cell that undergoes meiosis I, two daugher cells are produced, whereas for each cell that undergoes meiosis II, four daughter cells are produced*
D. is correct
A. true there is an opportunity for crossing over have in meiosis I that do npt have in meiosis II, in meiosis I hte homologous chromosomes are pairing up with each other, for crossing over to occur needs ot happen btw homologous chromosomes, which then separate and when go to meiosis II couldnt have crossing over because only have 1 copy of chromosome I and one copy of chormosome 2 so these are haploid cells!!! so no crossing over is possible! crossing over can only occur in dipploid cell becuase you need members of ht epair to cross over with each other
B. true- need centromeres to divide when pulling apart sister chromatids** something happen in meiosis II, in meiosis I you are not breaking apart siser chormatids, dont have ot break centromeres takign one copy of chromosome I and one copy of chromsome I and spearatign them from each other
the testes
male primary sex organ, two jobs
- make sperm
- make testosterone
testosteorne
what type of hormone?
STEROID so if it is a steroid it will be hydrophobic!
so what that means is that if we ned this testosterone in order to have maximum viability with our sperm we will create our sperm in a very hydrophilic like environment we have a problem on our hands, once put it into our seminiferous tube it will be like man no i am out, im hydrophobic
so once get it inside sem. tubulue bind it to androgen binding protein since it will be hydrophilic****
sperm develops btw sustenacular cells**
sustencular cells
sustain sperm development by secreting nutrients sperm need to survive and secreting antrogen binding protein or ABP
spermatogenesis graph
remember spermatid is an immature sperm cell, doesn’t realy have a tail that can cause it to swim, need to have good swimming ability to make it up to teh female reproductive tract, havent formed any of the enzymes that will help in fertalization process and have nto gathered mitoncdhria atthe bse of the head of sperm*
spermatogenesis image 2
epididymis
sperm storage
secrete nutrients, gives swimming ability
vas deferens
- long musclar duct
- peristalsis for ejaculation
- enters body cavity
- site of vasectomy
urethra
carries urine and semen
diff for females who keep system separate, we do not mix in case of ht emales they will utilize urethra for both*
what is in semen?
accessory glands are adding these fluids, when think aboitu semen its a whole lot of nutritious (fructose) alkaline fluid
a. seminal vesicles- get energy from fructose, 60% total ejaculate volume
b. prostate gland- around 30% of volume, produces a mildly alkaline fluid* helps nutrielize female reproductive tract which is slightly acidic, sperm do not like ot be in an acidic environment if we want to have sperm survive and fertilize an egg we need to bring up that pH, so prostate gland produces slgihtly basic fluid to neutrlize female reproductive tract
c. bulbourethral glands- other name can possibly show up is Cowper’s gland; produces baout 4% of total ejaculate stuff and this will secrete fluid upon arousal reason it wants to do this is because on arousal potential that ejactulatin will take place, as we mentioned that urethra carries not only semen but also in between bladder meaning some reminants in urine urethra, urine is slightly acidic because of high content of those hdyrogen ions so what the male wants to do to make sure urethra doesnt kill off sperm upon arousal eecrete alkaline mucus gets rid of any urine left behidn so that sperm will not be damaged as go through* so neturalizes acids that remain in teh urethra also will help lubricate urethra so have an easier passage of semen* so muscus lubricates urethra and neutralizes acid
gender development
formed week 7, what triggers development of male reprodutive system is if a testes forms or no
the presence of the Y chromosome triggers gender development*
the presence of the Y chromosome triggers mael development** (default is female) if do not form testes default form female reproductive system
what does progesterone and estrogen do?
estrogen ESTABLISHES and progesterone PROTECTS the endometrium***
so we keep endometrium protected by progesterone, why stays intact* so will have high progesterone*
image of aster microtubule, versus polar microtubule versus kinetochore microtubule
mitoic spindles separating sister chromatids during anaphase
The mitotic spindle at anaphase A. During anaphase A, the pairs of sister chromatids are separated and move toward the spindle poles. This occurs through the action of the kinetochore microtubules (illustrated in the inset). These microtubules shorten at their plus ends, while the motor proteins attached to the kinetochores of the chromatids travel toward the minus ends; thereby, the sister chromatids remain attached to the shortening microtubules.
As prometaphase ends and metaphase begins, the chromosomes align along the cell equator. Every chromosome has at least two microtubules extending from its kinetochore — with at least one microtubule connected to each pole. At this point, the tension within the cell becomes balanced, and the chromosomes no longer move back and forth. In addition, the spindle is now complete, and three groups of spindle microtubules are apparent. Kinetochore microtubules attach the chromosomes to the spindle pole; interpolar microtubules extend from the spindle pole across the equator, almost to the opposite spindle pole; and astral microtubules extend from the spindle pole to the cell membrane.
Metaphase leads to anaphase, during which each chromosome’s sister chromatids separate and move to opposite poles of the cell. Enzymatic breakdown of cohesin — which linked the sister chromatids together during prophase — causes this separation to occur. Upon separation, every chromatid becomes an independent chromosome. Meanwhile, changes in microtubule length provide the mechanism for chromosome movement. More specifically, in the first part of anaphase — sometimes called anaphase A — the kinetochore microtubules shorten and draw the chromosomes toward the spindle poles. Then, in the second part of anaphase — sometimes called anaphase B — the astral microtubules that are anchored to the cell membrane pull the poles further apart and the interpolar microtubules slide past each other, exerting additional pull on the chromosomes
microtubules image 3 (with plus signs)
What is the epididymis?
The epididymis is a long, coiled tube that rests on the backside of each testicle. It carries and stores sperm cells that are created in the testes. It’s also the job of the epididymis to bring the sperm to maturity — the sperm that emerge from the testes are immature and incapable of fertilization.
