Embryology Flashcards
advantages of sex
- Genetic variation- provides protection against a changing environment
disadvantages of sex
- Dilution of advantageous genes with those of another parent
- A partner must be found
gametes
spermatozoa and ova
cells that are set aside early in embryonic development to produce gametes
germ line
when are germ line cells set aside?
week 2 of embryonic development
what do seminiferous tubules consist of?
- myoid cells
- spermatogonia (germ line stem cells undergoing mitosis)
- spermatocytes (1 and 2)
- spermatids
- maturing sperm released into lumen
- leydig cells
- Sertoli cells
cells that are responsible for testosterone production
leydig cells
when does male mitotic proliferation begin?
puberty
sertoli cells
- release mature spermatozoa
- continuous tight junctions between these cells to prevent an immune reaction
- Damage to these junctions results in infertility as sperms would be destroyed, as can mumps (uncommonly).
subfertility sperm rate
below 2x10^7/ml
Typical sperm content in semen
10^8/ml
spermatogenesis order
spermatogonia- 1 spermatocytes (undergo meiosis 1)- 2 spermatocytes (undergoing meiosis 2)- future spermatozoa
spermatozoa path after leaving sertoli cells
passively flow to epididymis which secretes molecules in seminal fluid which activates them and allow them to swim
what stage is mitosis paused at for female babies?
prophase 1, at this stage they are primary oocyte surrounding by granulosa cells
what hormone does the pituitary gland produce?
follicle stimulating hormone (FSH) at puberty
what happens after follicles resume development after receiving FSH?
- Primary oocytes in follicles enlarge and synthesis RNA
- produce a glycoprotein zona pellucida around the oocyte and the granulosa layer proliferates (granulosa cells produce oestrogen to stimulate production of uterine lining), surrounded by theca layer.
- Granulosa cells communicate via gap junctions and fill the oocyte with antral fluid
what hormone binds to thecal cells and causes maturation into a Graafian (pre-ovulation) follicle?
luteinising hormone (LH), allows completion of meiosis 1 and arrests again in meiosis 2
where does the oocyte go after detached from granulosa?
out of ovary to the Fallopian tube and remains of the ruptured follicle become corpus luteum (produce progesterone and oestrogen to develop uterine lining)
when is meiosis 2 completed?
when fertilisation occurs
capacitation process in fertilisation
Proteases in cervical fluid remove the glycoprotein coat acquired in the epididymis by sperm which renders the cell membrane more permeable to calcium ions and therefore enables tail lashing and destabilises the membrane of the acrosome
in capacitation, what does cervical mucus modification during the menstrual cycle do?
allows sperm past the cervix, they can bind to the epithelium at start of the oviduct until ovulation
acrosome reaction in fertilisation
when sperm meets zona pellucida of egg, membranes of the acrosome and egg fuse so contents of acrosome can digest the ZP. It burrows towards the oocyte and fuses with its membrane causing repeated waves of calcium entry
what does the acrosome reaction do?
- Releases cortical granules that makes the ZP impenetrable to other sperm (ensuring one time fertilisation)
- Recommences meiosis 2 in the oocyte, producing a second polar body
what is produced at the end of fertilisation?
a zygote
reasons for assisted fertilisation
advancing maternal age, blocked vas efferentia/deferentia, impotence, low male fertility (<2x10^7 sperm) or blocked/absent oviducts
stages of assisted fertilisation
- promoting oogenesis involving exogenous FSH or blocking oestrogen detection to stimulate endogenous FSH production
- Eggs and sperm to be used are then harvested and sperm are artificially capacitated, they are mixed and observed (genetically tested) and then implanted
intra-cytoplasmic sperm injection
sperm are removed from the testis and injected directing into an oocyte if they are unable to succeed at above process
cleavage
mitosis where clump of cells stays same overall size
what happens at 4 cell stage?
- blastocyst starts to synthesis own mRNA and enzymatically destroys maternal mRNA
- Cells switch on an adhesion molecule and clump together hard
where does the blastocyst go after hatching out of zone pellucida?
down the fallopian tube to uterus, trophoblast invades the uterine epithelium in implantation
formation of hypoblast and yolk sage
- layer of ICM in contact with the fluid is the hypoblast
- some cells migrate down to edges of cavity to form yolk sac
formation of amniotic cavity and epiblast
layer of remaining ICM touching hypoblast detaches from rest of ICM and drops to form the amniotic cavity, this dropped layer is called the epiblast (becomes the baby
production of body axis
cells in the centre of the hypoblast produce the Hex protein and these move out towards the edge of the disc as a clump
formation of primitive streak in epiblast layer
clumped cells secrete proteins that oppose production of a primitive streak in the epiblast layer above so epiblast cells furthest from the clump pile up to give a primitive streak (spine precursor) and moves towards the centre to form a node while cells above the clump will form the head
gastrulation
- process of making gut (open central tube)
- after notochord is formed embryo lengthens and so endoderm becomes a long tube with yolk sac connected by a branch, the lungs, liver and pancreas later branch from the gut
formation of ectoderm and endoderm
- epiblast cells fall down from streak and squeeze into midline of the hypoblast to make an endoderm (“inner skin”) and others spread out between discs as a mesoderm (layer between ectoderm and endoderm)
notochord formation
- an aggregation of cells in middle of lower endoderm rises up as a notochord plate and then break off to form a notochord
neurulation
- produced of CNS (closed central tube)
- dorsal ectoderm folds inwards to give off a neural tube (above notochord) and seal up again, sealing of two separate structures because they have two different cell adhesion molecules
problems if closure of CNS fails
spinal bifida or anencephaly (absence of a major portion of the brain, skull, and scalp) occur, v rarely a twin embryo may be caught up in this closure and engulfed creating abnormality fetus-in-fetu
neural crest
ectodermal cells in gap above neural tube
migrates towards organs and these processes become the PNS, adrenal gland & melanocytes in skin
somites and formation
segments on either side of neural tube, precursors to vertebrae and skeletal muscle
formed by division of mesoderm around neural tube
differentiation
signals spread to neighbouring tissues to switch on other genes in them and cause them to specialise, these differences ripple out throughout body to produce different cell types
tissue migration of neural crest cells
Neural crest cells come from the back of the head where they meet the facial centre line
tissue migration of secondary cleft palate
if secondary cleft palate which seals nose and mouth do not seal, cleft palate occurs
stages where monozygotic twins can arise:
- if two blastocyst cells produced after first division of cleavage lose contact with each other= two embryos implant separately in womb, separate placentas
- if newly created ICM splits into two separate clumps within trophectoderm= twins share a placenta but have separate amnions (most common), risk of foetal transfusion syndrome (one twin takes more nutritional supply than the other)
- if two primitive streaks form in the epiblast= produces twins with same amniotic cavity (likely conjoined), less commonly- primitive streak may split and embryo has two heads
which gland produces growth hormone?
pituitary gland
pituitary tumours making excess GH=
gigantism
how can tissues relay GH signals to other cells?
insulin growth hormone
only growth in body that GH affects directly
liver and muscle growth
Laron syndrome
cells have no receptors for GH, so body is smaller but with Vitruvian proportions
what allows correction of mistakes and knowing when to cease growth?
feedback loop of growth signals
limb growth
Limbs know what size they are meant to be, fast growth can occur at any time, two paired limbs grow independently
- occurs v quickly needs rapidly growing vascular system to support oxygen needs→ anything that inhibits blood vessel growth will impair limb growth and permit non-Vitruvian conditions
bone growth
Bones know when to stop growing as they lose ability to respond to GH with increasing divisions
thalidomide use and disease
prescribed for morning sickiness but found to kill developing blood vessels → foetuses only grew short limbs (phocomelia)
achondroplasia
mutation stopping proper development of chondrocytes (cartilage cells) resulting in individuals with average sized trunk and short limbs
Epiphyseal plates (growth plates)
made of hyaline cartilage, found near end of long bones in children, large bones grow slower than short ones as they are further from cells deep in the growth plate
Skin growth
not controlled by genetics, where skin is stretched, mitosis occurs to reduce tension
androgen insensitivity syndrome
if androgen receptor in an XY embryo doesn’t work, exterior default female features will be present but with male gonads as rest of body cannot detect male hormones
when do embryos start to express gender
when gonad growth commences
gonadal formation in embryogenesis
• Germ line cells are removed from the epiblast to the yolk sac (outside the body), aren’t involved in gastrulation, they migrate from the yolk sac, through gut and mesentery (sheet of tissue that connects gut to cavity wall) to the gonadal ridge
which gene determines gender
SRY gene on Y chromosome, somatic cells of gonad must express SRY to be male
SRY effect on gonads
Switched on SRY gene make gonadal somatic cells become testes (instead of ovaries) that secrete androgenic hormones → sole signal to rest of body to become male
androgenic hormones
testosterone and anti-Mullerian hormone (AMH)- destroys early oviducts and uterus
What are non-gonadal somatic cells influenced by?
androgenic hormones
what is testosterone concentred by to become an effective ligand?
5α reductase to form 5a-dihydrotestosterone
guevodoces
Children with deficient 5α reductase (due to mutation) have female bodies before puberty.
At puberty, when level of testosterone is high enough to stimulate androgen receptors sufficiently (even without enzyme) they become young men
source of SHH signals
notochord
