Gametogenesis Flashcards
what are epigenetic effects (3) main points
- non-DNA changes
- can affect gene expression
- can influence lifetime outcomes
what are the gonads
- ovaries
- testes
where do the gonads develop
at the genital ridge
which migrating cell populations give rise to the gonads. which also multiply?
- primordial germ cells - these also multiply
- germinal epithelial cells
- mesonephric cells
what are gonads
specialised organ that produces the gametes (sperm or oocyte / egg) and sex hormones of organism
where do the cell populations that give rise to gonads go
they migrate to the genital ridge
what determines if testes or ovaries (gonads) develop
what chromosome sperm is carrying
- X chromosome -> ovaries develop
- Y chromosome -> testes develop
why does Y-chromosome carrying sperm result in testes
SRY gene on Y chromosome (sex-determining region of Y chromosome) ‘makes’ a testis
what chromosome is the egg carrying?
X chromosome
what are the gamete precursors
primordial germ cells
what are gametes
- sperm
- oocyte (immature egg cell) or egg
from the cell populations that give rise to gonads which do and don’t contain SRY gene
germinal epithelial cells express SRY
primordial germ cells and mesonephric cells do not express SRY
what do the cell populations that give rise to the gonads contribute to in testis formation
- primordial germ cells -> gamete precursors: give rise to sperm and egg
- germinal epithelial cells -> give rise to primitive sex cords and Sertolli cells that enclose the primordial germ cells (prespermatogonia)
- mesonephric cells -> give rise to the vasculature, Leydig cells, seminiferous tubules
what is spermatogonia
- spermatogonia = germ cells responsible for producing sperm cells (spermatozoa) thru spermatogenesis
what do Leydig cells produce
androgens (male sex hormones; class of steroid hormones) - incl testosterone, DHT
what do the cell populations that give rise to the gonads also contribute to in ovary formation
- primordial germ cells -> gamete precursors: give rise to sperm and egg
- germinal epithelial cells -> cluster around PGCs (oogonia) to form primordial ovarian follicles
- mesonephric cells -> give rise to the vasculature, stroma
what occurs after gonad formation
internal genitalia
how do internal genitalia form
two unipotential primordia (organ/tissue in earliest stage of development) located next to gonads give rise to internal genitalia
- unipotential - ability of primordia to give rise to a specific type of organ or tissue not into multiple types; here: two early developmental structures specialised and predetermined to develop into internal genitalia only
what 2 main hormones to foetal testis (gonads) make & their function
- androgens in Leydig cells -> stimulate Wolffian ducts (male) to make epididymis, vas deferens, prostate
- anti-mullerian inhibitor (AMH) in sertoli cells -> causes mullerian ducts to regress (preventing formation of female internal reproductive structures)
what is the role of the mullerian ducts
- arise during early embryonic development
- paired embryonic structures
- present in both male and female embryos
- crucial role in development of reproductive system, esp in females
what happens to mullerian ducts in females
absence of AMH, mullerian ducts become oviducts, uterus, cervix, upper vagina
what occurs after internal genitalia formation in males
- external genitalia form in presence of androgens
- bipotential precursors become scrotum and penis in
- bipotential precursors: structures in early embryonic development that have potential to differentiate into either of 2 distinct cell types
gametogenesis same but different
- gametogenesis is process of producing gametes
- spermatogenesis in males & oogenesis in females
- meisosis of spermatogonia and oogonia - into mature gametes - sperm or eggs- capable of fertilisation ie/ diploid cell (46) reduced to haploid cell (23)
BUT timing is different
how is gametogenesis different explanation
- sperm produced continuously from puberty until death (decline in sperm quality overtime) ; spermatogenesis occurs at puberty
- oogenesis starts before birth => number of oocytes (potential eggs) fixed at birth. Oocytes suspended at Prophase 1 in meiosis at birth until puberty
- meiosis resumes at ovulation (continues till most oocytes been ovulated or lost to atresia)
- meiosis completed following fertilisation (ovulated oocyte that’s fertilised)
=> 99% oocytes do not ovulate and lost through atresia (oocyte not chosen each menstruation) by time of menopause (~50yrs old)
connect epigenetics to tissue type
- each cell in body contains same genes
- various cell types due to different expression of these same genes
how is expression of same genes different (epigenetics)
- some genes imprinted ie/ only maternal or paternal copy expressed - seen in many genes for growth and development eg/ IGF2 gene
- no DNA changes / “marks” in gene expression come thru various processes such as methylation, histone modification, RNAs
methylation in epigenetics
formation of methyl groups on DNA -> prevents those genes from being transcribed and expressed
histone modifications in epigenetics
histone proteins wrap DNA up
depending on how tightly wrapped -> whether genes transcribed and expressed
- more tight => prevents
- loose wrapped => more open
when do epigenetic changes in methylation occur?
during gametogenesis, embyro development and foetal development
affecting lifetime gene expression
natural rise and drops on oocyte growth to embryo gene activation
what can also influence pattern of gene expression in epigenetics
- external factors such as environment (eg/ pollutants), lifestyle (eg/ exercise), alcohol and diet and smoking
- intergenerational effects in utero on oocytes and sperm and embryos
- WW2 dutch famine
explain intergenerational effects in utero on oocytes, sperm, embryos
at time that oocytes forming (w/ patterns of demethylation and re-established methylation) other modifications during embryo development - they not only affect the foetus being born but also their children as it is also the time that the gonads are forming
explain dutch famine on epigenetics
pregnant women were severely malnutrition which we saw affects in those children and their children
due to effects of malnutrition on gametogenesis and embryo development
what can the pattern of gene expression in epigenetics influence
- increased risk of major disease including hypertension, heart disease, obesity
- for the ‘developmental origins of adult disease’
what are the things in IVF that we do which can affect gene expression
hormonal stimulation, culture embryos
what is the result of the effects IVF can have on gene expression
- increase in some imprinting defects / birth defects esp Beckwith-Wiedemann syndrome and Angelman syndrome
- BWS characterised by overgrwoth of certain congenital features seen in children and increased risk of childhood cancer
