Devo Week 2

Front 1

2 classes of gene cascades

Back 1

maternal effect genes: expressed before fertilization, encode basic developmental features (e.g. body axis formation)

zygotic genes: supersede influence of maternal effect genes (e.g. hox)

Front 2

Three key concepts that guide developmental program

Back 2

Location

time

concentration gradients

Front 3

RNA polymerase II

Back 3

binds core promoter with aid of general transcription factors

Transcription factor TFIIH phosphorylates RPII to release it from the promoter.

Front 4

enhancer

Back 4

sequence to which transcription factors bind

functions in helping uncoil chromatin

Front 5

transcription factors

Back 5

2 domains: DNA binding domain and an activation domain that interacts with RNA polymerase

work in concert with co-activators to modulate chromatin structure

strategies: acetylation of histone tails (makes them negative); methylation, etc.)

Front 6

nucleosome

Back 6

protein core with DNA wound around its surface. Core is octamer with 2 copies of 4 different histones (H2A, H2B, H3, H4). histones positively charged, so they bind negatively charged dna

Front 7

epigenetic modifications

Back 7

influence gene expression through mechanisms not encoded by DNA.

e.g. acetylation/methylation of histones or DNA

Front 8

Wilm's tumor gene

Back 8

WT1

Repressor expressed in develping kidney. Homozygous recessive children develop kidney tumors early in life. WT1 is supposed to repress transcription of EGR-1, a transcription factor.

Front 9

Morphogens

Back 9

diffusible molecules, often described by their concentration gradients that specify or restrict fate of exposed cells.

--time dependent concentration gradients

--cells affected by their location and by whether or not they have receptor to respond

Front 10

morphogen examples

Back 10

retinoic acid

transforming growth factor B(eta)

bone morphogenic proteins (BMP4)

Sonic hedgehog (SHH)

Wnt/beta-Catenin

Front 11

Retinoic acid

Back 11

--critical for anterior-posterior axis formation of the embryo
--derived from Vitamin A
--excess OR deficiency leads to dysmorphogenesis
--changes Hox gene expression patterns
--mechanism: diffuses across membrane to bind RA receptors; these receptors then act as transcription factors that bind RA response elements; alter hox gene expression.
--e.g. too much RA, only trunk genes expressed; no head will develop

Front 12

Master genes and Nested gene expression

Back 12

Hox genes regulate activity of many downstream genes-->master control genes

mutations can cause large scale developmental effects

Front 13

HOX gene mutations

Back 13

human synpolydactyly from HoxD-13 mutations

Cardiac arterial septal defects and lissencephaly (nervous system malformation)

Front 14

Transformation Growth Factor Beta/Bone Morphogenic protein

Back 14

--members of family important for development of epithelial cells, lung, kidney, bone, and regulation of cell division and cell death.

--bind to receptor-->trans phosphorylation of receptor kinase-->phosphrylation of intracellular Smad proteins (transcription factors)

Front 15

Sonic hedgehog

Back 15

--Shh protein is a secreted morphogen that plays critical role in early embryonic patterning, migration, and differentiation.

--needs cholesterol to be active

-Receptor: Patched; in presence of Shh, patched stops repressing Smoothened (Smo); Smo leads to translocation of transciption factor Gli

--Shh-->Patched-->Smo-->Gli

Front 16

mutations of SHH or Patched

Back 16

holoprosencephaly (fusion of anterior side?), anophtalmia, cyclopia, polydactyly

Front 17

Wnt

Back 17

Drosophila gene wingless

--family plays role in proliferation, apoptosis, fate specification, migration, cancer

--in presence of Wnt, Beta-catenin (transcription factor) isn't degraded but rather enters nucleus to regulate expressoin

-problems: affect cardiac outflow tract, somite segmentation, neural tube formation, cancers

Front 18

Notch/Delta pathway

Back 18

--essential for lateral inhibition between cells during cell fate determination. big role in organ development--correct cell numbers and differentiation of progenitor cells.

--Notched receptor-->binds jagged ligands (Delta)-->releases intracellular domain (NICD)--> induces transcription factor HLH

Front 19

Receptor Tyrosine Kinases

Back 19

activate intraceullulr signaling pathways

growth factors such as insulin, nerve growth factor, etc. bind these receptors

--cell proliferation, migration, survival, cancer

Front 20

transcription factors

Back 20

-can directly bind dna, or repress or enhance other transcription factors

Front 21

Pax genes

Back 21

master gene for eye development

-problem: Waardenburg's syndrom type 1 result of mutation

Front 22

Basic Helix-Loop-Helix transcription factors

Back 22

bHLH: regulatie cell differentation in many tissues.

e.g. MyoD for differentiation into muscle

Front 23

induction

Back 23

inducer cells sends signal to a responder which causes change in cell fate.

capacity to respond known as competence. sometimes requires activation by competence factor.

--occurs frequenty between mesenchym and epithelial cells

--reciprocal interactions underlie mutual differentiations

Front 24

Induction of neural precursor cells

Back 24

BMP4 made by ectodermal cells, secreted. when it binds ectodermal cells, leads to epidermal specific genes and inhibits neural phenotype.

--organizer secretes noggin, chordin, and follistatin to prevent BMP4 from binding the ectoderm near the organizer, elading to neuronal differentiation.

Front 25

Neural tube differentiation

Back 25

Dorsal-ventral axis of neural tube determined by gradients of BMP4 and SHH

Dorsal: BMP4 secreted by ectoderm and neural tube roof plate

Ventral: SHH secreted by notochord and ventral neural tube floor plate

opposing gradients control fate of neuroblasts in developing neural tube

high SHH, low BMP-->motor neurons; opposite-->sensory neurons

Front 26

Teratogens

Back 26

disrupt normal development

RA: physical anomalies, accutane

Thalidomide: sedative given to pregnant women that increased congenital abnormalities enormously. inhibits angiogenesis-->phocomelia (no long bones in the limbs), heart defects, absence of external ears, malformed intestines

Front 27

Gastrulation

Back 27

bilaminar disc (epiblast and hypoblast) becomes a three layer tri laminar disc (aka the gastrula) containing all three germ layers

body axes become firmly established

Front 28

Primitive streak

Back 28

15 days: thick band of epiblast cells appears on caudal, median plane. proliferates and stretches towards the cranial end, where it bulges to from the primitive node (aka Henson's node) with cilia on its ventral surface

--primitive groove and primitive pit form through invagination of epiblast cells.

--primitive streak invovled in formation of mesoderm and endoderm until early week 4; it then reduces in size to become part of sacrococcygeal region and disappears completley by end of week 4

Front 29

Formation of three germ cell layers

Back 29

epiblast cells migrate through primitive streak and pass under it, forming mesenchyme.

--epiblast, primitive node, and portions of the primitive streak cells displace the hypoblast and form innermost layer of embryo, called endoderm; outermost layer of epiblast cells renamed ectoderm

--cells that subsequently move inward through primitive streak and node settle between the two layers to form the mesoderm, which eventually occupies most of the space between the two layers

Front 30

mesenchyme

Back 30

amoeboid and actively phagocytic cells suspended in gelatinous matrix.

--forms most of the CT of the embryo

--some become mesoblasts and will form the embyronic mesoderm

Front 31

prechordal plate

Back 31

during formation of the three germ layers, at the cranial end ectoderm and endoderm remained fused. This will become the oropharyngeal membrane, the future site of the oral cavity

Front 32

cloacal membrane

Back 32

during formation of the germ layers, ectoderm and endoderm that remains fused at the caudal end will become this emmbrane, the future site of the anus

Front 33

Establishment of body axes overview

Back 33

both before and during gastrulation
3 axes:
cranio-caudal
dorsal-ventral
left-right

Front 34

formation of cranio caudal axis

Back 34

signaled by the ANTERIOR VISCERAL ENDODERM, or AVE located at the cranial margin of the bilaminar disc.

--expresses genes essential for head formation (transcription factors OTX2, LIM1, HESX1, and secreted factor Cerberus)

--primitive streak is initiated and maintained by local expression of Nodal, a member of the TGFBeta superfamily

Front 35

Formation of the dorsal ventral axis

Back 35

Specified through interactions between BMP4 and various factors secreted by primitive node.

-BMP4 secreted throughout embryonic disc. in absence of opposing signals, would cause all mesoderm to become ventralized

--genes expressed by primitive node (aka organizer) allow for dorsalization of mesoderm by antagonizing BMP4

--secretion of chordin (activated by tf Goosecoid), noggin, and follistatin by primtiive node enabled cranial mesoderm to become dorsalized to form notochord, somites, somitomeres. these three genes are subsequently expressed by notochord and play role in neural induction

--over or under expression of goosecoid-->malformations of the head

Front 36

Formation of the left-right axis

Back 36

--established during gastrulation
--Fibroblast growth factor 8 (FGF8) induces expression of Nodal only on left side. Ventral ciliated surface of primitive node beats to left and creates Nodal gradient on left side.
--FGF8 maintains expression of Nodal and Lefty-2 in lateral mesoderm, which up regulates PITX2-->tf that estbalisshes left sidedness and is expressed on left side of heart stomach, and primitive gut

--Lefty 1 is expressed on left side of floor plate of develping neural tube-->prevents left specific signals from crossing to right side

-Brachyury gene, secreted by developing notochrod, essentail for expression of Nodal, Lefty1 and 2

-right side not well understood, tf Snail may play some role

Front 37

Situs inversus

Back 37

body's internal organs are transposed to theo pposite side

Front 38

Kartagener Syndrome

Back 38

primary ciliary dysplasia

-autosomal recessive
-cilia lining respiratory tract and flagela of sperm missing or malfunctioning. approximately half of these patients have situs inversus

Front 39

Fate map of epiblast cells

Back 39

Depends on where tehy pass through primitive streak/node.

Top of node, paraxial mesoderm (somites and somitomeres)

next portion form intermediate mesoderm (urogenital system)

more caudal portions form lateral plate mesoderm (body wall)

most caudal portion form extraembryonic mesoderm (chorion)

Front 40

Gastrulation tumors

Back 40

remnant of primitive streak remains and becomes sacrococcygeal teratoma. contains many types of tissues

Front 41

sirenomelia

Back 41

aka caudal dysgenesis

-gastrulation very sensitive to teratogens. often insufficient mesoderm forms in caudal region. often results in fusion of the lower limbs or holoprosencephaly

Front 42

notochord

Back 42

basis for development of axial skeleton, indicates future site of vertebral bodies, gives embryo some rigidity

--forms during gastrulation, induces overlying extoderm to form the neural plate and synchornizes the development of the neural tube

Front 43

formation of the notochord

Back 43

notochordal process forms wihting developing mesoderm from cells migrating from primitive pit. grows in a cranial direction until it reaches the prechordal plate.

--primitive pit extends into notochrodal process, develops a lumen, and becomes the notochordal canal

--day 19/20, notochordal process fuses with underlying endoderm, then fused layers break down, producing a temporary communication between the amniotic cavity and the umiblical vesicle (neuroenteric canal)

--remaining roof of notochordal process form notochord plate, which folds ventrally to become the tubular notochord. buried in mesoderm with underlying endoderm.

Front 44

neurenteric fistula

Back 44

neurenteric canal extends into adulthood. bacteria can pass from gut into vertebral column/nervous system.

--if partially closed, may result in neurenteric cyst

Front 45

chordomas

Back 45

slow growing tumor from remnant of notochord. found in cranial and nasopharyngeal regions

Front 46

Formation of the neural tube

Back 46

Neurulation: notochord functions as an inducer, intiaiting the overlying ectoderm to form and elongated plate of thickened epithelial cells called the neural plate

--neural plate broadens and eventually expands beyond limits of the notochord. at day 18, invaginates along its central axis to form a median groove (neural groove) flanked by two neural folds. By end of third week, neural folds fuse to form the neural tube. FUsion begins in cervical region and proceeds cranially and caudally.

--anterior and posterior neuropores remain open to communicate with the amniotic cavity. Close on days 26 and 28. Closure complete by end of fourth week

--neural tube extends only through somite 31; inferior and sacral regions of neural tube form independently

-ectoderm of hte neural plate (neuroectoderm) will give rise to the CNS

Front 47

Secondary neurulation

Back 47

process by which pluripotent tissue from the caudal eminence forms a solid neural cord that develops a lumen and joins with rest of the neural tube by day 40

Front 48

neural crest cells

Back 48

as neural tube separates from surfae exctoderm, some neuroectodermal cells detach and give rise to neural crest.

some will form dorsal root ganglia, other will no differentiate immediately and move throughout embryo. precursors to: ganglia of ANS; pharyngeal cartilages and other CT in head; pigment cells; adrenal medulla

Front 49

Ectoderm

Back 49

Differentiaites into surface and neuroectoderm

Front 50

Surface ectoderm

Back 50

epidermis
mammary glands
sbucutaneous glands
hair
enamel
pharyngeal arch cartilages
adrenal medulla

Front 51

neuroectoderm

Back 51

neural crest
neural tube

Front 52

paraxial mesoderm

Back 52

-mesoderm close to the midline
--condesnes into paired, loosely organized somitomeres (add 3-4 per day)
--appear in cephalic region and develop cranially and caudally
--first seven pairs-->musculature of face, jaw, and throat
--somitomeres 8,9,and 10 becomes first, second, and third pairs of somites
--end of week 5, 42-44 somite pairs, but caudal most will degenerate, leaving 34 or 38 pairs
--somites give rise to most of axial skeleton, determine segmental organization, voluntary muscles, part of dermis

Front 53

intermediate mesoderm

Back 53

termporarily connects paraxial mesoderm with lateral mesoderm
-->urinary system, portions of gonads, parts of male genital duct system

Front 54

lateral mesoderm

Back 54

--coelomic spaces coalesce and form horse-shoe shaped intraembryonic coelom that will give rise to thorax and abdomen cavities. splits mesoderm into two layers:

splanchnic/visceral mesoderm: ventrall located, gives rise to the coverings of the visceral organs; continuous with extraembryonic mesoderm covering the yolk sac

--somatic or parietal mesoderm (dorsal): continous with extramembryonic mesoderm covering the amnion. somatic mesoderm gives rise to the body wall, parts of the limbs, most of the dermis

Front 55

Endoderm

Back 55

first set of epiblast cells through the groove/pit displaces hypoblast and becomes innermost layer

--forms future digestive system, epithelial lining of repsiratory system, parenchyma of glands, epithelial lining of urogenital system, and epithelial lining of various pharyngeal pouches

Front 56

Origin of placental tissues

Back 56

Maternal: derived from the endometrium of the uterus

Fetal: from the trophoblast and its successors (cyto and syncytiotrophoblast, and the villous chorion)

Front 57

Early Placental development

Back 57

Begins with implantation. hCG produced by syncytiotrophoblast; blastocyst prevents prostaglandin release (which would decrease progesterone); prevents production of HLA antigens

--blastocyst initially sustained by uterine secretions, but will soon need support from early placental tissues

--fetal part of the placenta begins as the syncytiotrophoblast invades the endometrium of the uterus. by day 9, lacunar spaces develop, fuse, and intercommunicating network begins. By days 11 and 12, early uteroplacental ciruclation as maternal blood flows into lacunae

next will be chorionic villi

Front 58

The Decidual reactions

Back 58

endometrial connective tissue cells begin a transformation. The endometrial stroma cells surrounding the implantation site become loaded with glycogen and lipids and develop a polyhedral shape

--these decidual cells then degenerate, undergoing apoptosis, and syncytiotrophobolast engulfs them, providing rich nutrients for the developing embryo. Maternal blood and uterine secretions add to this nutrient source

--also provides an immunologically protected site for hte ocnceptus

Front 59

Decidua of the endometrium

Back 59

the functional layer of teh endometrium in a pregnant woman. Three regions:

Decidua basalis: part deep to the conceptis. forms the maternal part of the placenta

decidua capsularis: superficial part overlying the conceptus. eventually disintegrates

decidua parietalis--all of the remianing decidua

Front 60

Development of the chorionic villi

Back 60

Primary chorionic villi induced by extraembryonic mesoderm. These are outgrowths of cytotrohpobolasts into the syncytiotrohpoblast which grow out into the blood filled lacunae

secondary chorionic villi at about 15-16 days post fertilization, characterized by extraembryonic mesoderm penetrating core of primary villi

tertiary chorionic villi at about 20-21 days post fertilization with differentiation of mesenchyme into capillaries and blood cells. form network that will eventually be connected to the embyrnoic heart through vessels in chorion and connecting stalk

--by end of 3rd week, embryonic blood flowing and exchanges taking place

--by end of 4th week, complex vascular network establishedi n the placenta

--chorionic villi cover enter chorionic sac until beginning of 8th week; some areas degenerate and other persist in the area where the chorion is associated with the decidua basalis

Front 61

Chorionic villus sampling (CVS)

Back 61

prenatal diagnosis. Performed between 10 and 12 weeks

compare with 15-18 weeks for amniocentesis. however, amniocentesis is safer; risks include miscarriage, infection, and amniotic fluid leakage

Front 62

placental septa

Back 62

wedge shaped areas of decidual tissue created by invasion of chorionic villi; these septa divide the fetal part of the placenta into 10-38 irregular areas called cotyledons; each cotyledon consists of 2 or more villi and branches; give the placenta its cobblestone appearance

Front 63

smooth chorion (Laeve)

Back 63

area where chorionic villi are compressed and degenerate due to the expansion of the embryo into the uterine cavity

aka the abembryonic sideo f the chorion

Front 64

Villous chorion

Back 64

aka chorion frondosum

embryonic side of the chorion where the villi actually increase in number and branch profusely.

along with the development of the smooth chorion, the chorion frondosum's persistent growht results in teh placental disc shape

forms the fetal part of placenta; connected to the maternal part by an extension of cytotrohpoblastic cells through the syncytiotrophoblast.

Front 65

cytotrophoblastic shell

Back 65

formed by extensions of the cytotrophoblast through the syncytiotrophoblast; gradually surrounds the chorionic sac and attaches it to the endometrium. maternal blood vessels pass through and open into the intervillous space

Front 66

intervillous space

Back 66

originates from the lacunae in the syncytiotrophoblast that formed in week 2. divided into compartments by placental septa, but communication exists between the compartments. Filled with amternal blood, which showers the branch villi -->site of fetal/maternal exchange

Front 67

amniochorionic membrane

Back 67

formed from fusion of amnionic membrane and the chorionic sac (due to much faster growth of amnion); eventually fuses wit hteh decidua capsularis, and later, with teh decidua parietalis. This si the membrane that ruptures when a woman's water breaks.

Front 68

PROM

Back 68

premature rupture of amniochorionic membrane is most common cause of premature labor

Front 69

placental membrane

Back 69

prevents mixing of maternal and fetal blood

Front 70

Fetal placental circulation

Back 70

Deoxygenated blood leaves fetus via 2 umbilical arteries to placenta; divides into various chorionic arteries which branch in chorionic plate and enter villi

blood returns to fetus via 1 umbilicial vein

Front 71

Maternal placental circulation

Back 71

enters intervillous psace through 80-100 spiral endometrial arteries; jets twoards chorionic plate and through gaps in cytotrophoblastic shell

--blood reaches the decdiual plate and exits through endometrial veins back to the maternal circulation

Front 72

IUGR

Back 72

intrauterine growth retardation

due to decrease in uteroplacental circulation that causes hypoxia

Front 73

Pre-eclampsia

Back 73

hypertension that arises in pregnancy; associated with significant amounts of protein in urine

many different caauses of syndrome.

theory is that placenta releases some substance that causes maternal BV disfunction

no known cure but birth

Front 74

placental membrane con't

Back 74

seaprates maternal and fetal blood; formerly called a barrier, but not accurate b/c a majority of substances pass through it freely

--exchange of gases, hormones, electroyltes, antibodies, co2, urea, uric acid, bilirubin

--some hormones pass through freely, for example, synthetic progestins, which masculinize a fetus. synthetic estrogens can easily cross, and can cause cancers

Front 75

placental membrane layers

Back 75

until 20 weeks, 4 layers:
endothelial lining of fetal blood vessel, connective tissue in villus core, cytotrophoblastic later, syncytiotrohpoblast;

after 20 weeks:
cytotrophoblastic cells become very thin and even disappear in some areas. leads to direct contact of syncytio- and endothelium of fetal capillaries. passing of both maternal and fetal RBC, maternal leukocytes, bacteria nd protozoa can create defects and pass through

Front 76

fetal erythroblastosis

Back 76

anti-RH antibodies from mother due to small amount of fetal RBCs passing through the placental membrane

Front 77

other placental functions

Back 77

--synthesize glycogen, cholesterol, fatty acids during early pregnancy

--transfer of maternal antibodies

Front 78

syncytiotrophoblast hormone fxns

Back 78

--steroid hormones, estrogens, and progesterone produced
--protein hormones: hCG
-human chorionic sommatomammotropin
--human chorionic thyrotropin
--human chorionic corticotropin

Front 79

Fetal membranes

Back 79

four fetal membranes: amnion, chorion, yolk sac, and allantois. other than portions of the yolk sac and allantois, do not form part of the embryo

Front 80

chorion

Back 80

originates from trohpoblast and extraembryonic mesoderm

chorionic sac (formerly extraembryonic coelom) surround developing amnion and embryo and consists of syncytiotrophoblast, cytotrophobalst, and extraembryonic somatic mesoderm

Front 81

amnion

Back 81

originates from amnioblasts (which come from epiblast and line the amniotic cavity). grows faster than the chorionic sac and eventually obliterates the chorionic cavity. surround developing embryo and umbilical cord and fuses with chorionic sac to form amniochorionic membrane, then with decidusa capsularis and parietalis

Front 82

yolk sac

Back 82

aka umbilical vesicle
--originates from the hypoblast exocoelomic cavity
--nutrient transfer during weeks 2 and 3 while uteroplacental ciruclation established. plays a role in hemopoiesis prior to liver development. eventually becoems very small; dorsal portion incorporated into the primitive gut.

--VITAL as site of primordial germ cells during the third week

--atrophies and is usually invisible by week 20

Front 83

allantois

Back 83

outpouching wall of yolk sac that extends into the connecting stalk

importance:
1. blood flormation during weeks 3-5
2. allantoic blood vessels become the umbilical vein and arteries
3. intraembryonic portion of allantois runs from umbilicus to urniary bladder, forming the urachus. after birth urachus becomes fibrous cord known as the median umbilical ligament

Front 84

Amniotic fluid

Back 84

99%water. sampled by amniocentesis

most derived from maternal blood, but initially secreted by amniotic cells

volume changes with gestation; 30 mL at 10 weeks, at 37 is 800-1000mL

--fetus contributes through its respiratory and gi tracts, and at 11 weeks, by its urine

--permits symmetrical external growth and normal lung development
-prevents amnion from adhering to embryo
-cushions embryo
-enables fetus to move
-maintains homeostasis
-barrier to infection

Front 85

oligohydramnios

Back 85

low volume of amniotic fluid for gestational age

-most common reason is preamture rupture of amniochorionic membrane

-can also be a sign of renal agenesis and/or obsturctive uropathy

Front 86

polyhydramnios

Back 86

results from fetus not swallowing the normal amounts of fluid. associated with esophageal atresia or severe anomalies of CNS

Front 87

normal placenta at birth

Back 87

delivered 10 minutes after baby
-should be 22 cm wide and 2.5 cm thick
--should weigh about 470 grams, discoid shape

-should be complete and contain umbilical vessels
--shouldn't have accessory lobes, hemorrhage, tumors, or nodules

Front 88

placenta accreta

Back 88

abnormal superficial attachment of placenta to the myometrium (middle layer of uterine wall). puts women at risk of hemorrhage during childbirth. 3 forms:
1. most common is invasion of myometrium; does not penetrate entire muscle. 3/4 of all cases
2.Placenta increta: placenta extends further into myometrium
3. Placenta percreta: most severe; 5-7% of all cases; penetrates entire myometrium

Front 89

Placenta previa

Back 89

blastocyst implants clsoe to internal os, overlying the cervix. can cause bleeding; may need caesarean section

Front 90

Placenta abruptio

Back 90

premature sepration of hte placenta from the site of the uterin implantation before delivery of the fetus

Front 91

Gestational trophoblastic disesase

Back 91

group of diseases involving abnormal growth of cells of the trophoblast

--most common is hydatidiform mole; aka molar pregnancy. chorionic villi converted into a mass of fluid filled vesicles that may fill the uterus nad resemble a bunch of grapes

Front 92

complete hydatidiform mole

Back 92

sperm fertilizes empty egg. male genes influence placental growht. abnormal bleeding and high levels of hCG

-percentage of these may develop into choriocarcinoma. carcinoma of chorionic epithelium; very aggresive in metastasis, bleeds profusely. extremely sensitive to chemotheraphy

Front 93

Partial hydatidiform mole

Back 93

two sperm fertilize a normal egg. some fetal tissue mixed with trophoblastic tissue. no vialbe fetus formed. rarely develop into malignat GTD

Front 94

monozygotic twins

Back 94

1 in 85 pregnancies
early separation (2-8 cell stage)-->two amnionis, two chorions, two placentas
--separation at end of first week-->two embryos, two amnions, same chorionic sac and common placenta
--after 8 days-->single palcenta, single amniotic cavity
--beyond day 12-->conjoined twins (craniopagus, thoracopagus, ischiopagus, pyopagus, omphalopagus)