Developmental Biology Exam 2 Flashcards

1
Q

Primary sex determination

A

gonads: testees or ovaries
genetics

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2
Q

Secondary sex determiantion

A

Phenotype- male vs female internal and external organs
Hormones and paracrine factors from the gonads

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3
Q

Bipotential gonads

A

genital ridge: gonad rudiment will become gentile duct
bipotent: can become ovaries and testees
Have indifferent development takes place followed by differentiation into either testees or ovaries (based on XX and XY genotype
Have both Mullerian and Wolffian ducts
Hormones made by genotype will fully generate one duct and disintegrate the other

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4
Q

How genitals are affected with XY genotype

A

Gonads become the testees
Wolffian duct differentiates into sperm transport duct
Mullerian duct is degenerated

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5
Q

How genitals are affected with XX genotype

A

Gonads become ovaries
Mullerian duct becomes oviduct which become the fallopian tubes
Wolffian duct is degenerated

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6
Q

Primary Sex determination for XY

A

Gene SRY promotes testis formation
SRY is a transcription factor which binds enhancer region of Sox9 gene. Sox9 is then expressed by activating itself via SRY
Sox9 also activates anti-Mullerian hormone (AMH) and promotes degradation of beta-catenin.

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7
Q

Primary Sex determination for XX

A

no SRY gene present
wnt4 paracrine factor leads to wnt/beta-catenin signaling and target gene expression
wnt4 leads to beta-catenin stabilization
Results in expression of ovary differentiation genes
Beta-catenin promotes maintenance of ovarian structures and blocks expression of Sox9

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8
Q

Secondary sex determination female

A

Bipotential gonad leads to wnt4 factor leads to ovary leads to granula cells and thecal cells leads to follicles leads to estrogen leads to differentiation of Mullerian duct leads to female sex phenotype
In the absence of testosterone the Wolffian duct regresses

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9
Q

Secondary Sex determination male

A

Bipotential gonad leads to SRY, Sox9 leads to testees leads to:
1. Sertoli cells which make AMH which leads to regression of Mullerian duct
AND
2. Leydig cells which make testosterone which causes differentiation of Wolffian duct which causes male sex phenotype

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10
Q

Germ Plasma theory (1892)

A

Weismann proposed
Some germ cells contain heritable information and somatic cells carry out ordinary body functions
germ plasm, which is independent from all other cells of the body (somatoplasm), is the essential element of germ cells (eggs and sperm) and is the hereditary material that is passed from generation to generation.

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11
Q

Background of Test of Germ Plasma Theory (1910)

A

Done by Theodore Boveri
Used parascaris aequorum which is a round worm parasite with chunky chromosomes you can see under a microscope
Have two chromosomes per haploid cell
Cleavage of first embryonic development separates animal half from vegetal half of the zygote.
Animal chromosomes during first two blastomeres: chromosome diminution
vegetal blastomere: chromosomes remain normal
During second cleavage animal cells split meridionally and the vegetal cell divides equatorially. Both vegetal cells created have normal chromosomes
Therefore at the fourth cleavage only one cell (vegetal) will have a full set of genes
At the 16th cell stage there will only be two cells with undiminished chromosomes. One of them becomes a germ cell and the other does chromosomes diminution to form stomatic cell

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12
Q

Chromosome diminution

A

When chromosome blastomere ends fragment before cell division
Only portion of original chromosome survives
Genes are lost and are therefore not present in new nuclei

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13
Q

Meridional division

A

a type of cell division that occurs during the early stages of embryonic development when a furrow cuts through the center of an egg, bisecting both poles

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14
Q

Equatorial division

A

is a term used to describe the process of cell division where chromosomes are divided equally into two daughter cells during metaphase of mitosis or meiosis:

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15
Q

Test of Germ Plasma Theory (1910)

A

Boveri set out to study the part of the cell plasma that caused the chromosomes to not diminish and see if this so called section of the cytoplasm existed
He centrifuged the eggs before their first cleavage to shift orientation of mitotic spindle. Therefore each cell formed should have portion of the vegetal portion
After first division no nucleus underwent chromosomal diminution. Only the animal ones for the second division underwent chromosomal diminution.
He concluded the vegetal cytoplasm contains a factor that protects nuclei from chromosomal diminution and determines germ cells

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16
Q

Primordial germ cells (PGCs)

A

Germ cells (aka. germ line) = cells that make gametes. Totipotent
Germ cells derived from PGCs. Can become either sperm or eggs. Therefore PGCs are bipotent

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17
Q

Where do PGCs come from?

A

In mammals they come from the ICM
ICM made primitive endoderm. epiblast are all cells of the embryo which also make PGCs
On P side becomes PGCs and are more likely to be mesoderm but signals tell them they are going to be germ cells
Therefore induction occurs
Migrate to gentile ridge and during this migration the PGCs also proliferate

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18
Q

Mammalian spermatogenesis

A
  1. Proliferation
  2. Meiosis
  3. Differentiation
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19
Q

Spermatogenesis: Proliferative Phase

A
  1. primordial germ cells (PGCs) migrate to the gentile ridge. While migrating they become gonocytes. Once at destination they become seminiferous tubules
  2. Contact with the seminiferous tubules leads to gonocyte differentiation into spermatogonial stem cells (SSCs). SSCs are type A spermatogonia.
    The type A spermatogonia (stem cells) will either not divide, will divide to make asymmetric cell or through mitosis will make type B spermatogonia which will differentiate and mitosis to have two primary spermatocytes
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20
Q

sertoli cells

A

men mesodermal cells differentiate into these
Their role is to secrete AMH
Will also form seminiferous tubules
during week eight they surround germ cells to make testis chords

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21
Q

Testis chords

A

Form loops in central region of developing testis and are connected by thin canals called rete testis near developing kidney duct

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22
Q

What happens when male germ cells enter the gonads?

A

They develop within the testis chord, proliferate and then arrest in mitosis
When puberty hits, the testis cords develop into seminiferous tubules. The germ cells migrate to the periphery of the tubules to make SSC’s

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23
Q

Two directions men mesodermal cells can go?

A

Sertoli cells (epithelial) or Leydig cells (Mesenchymal)

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24
Q

Leydig cells

A

Secrete testosterone

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25
Q

What does fully developed testis have?

A

epithelial tubules of Sertoli cells surrounding germ cells and a mesenchymal cell population that secrete testosterone
To protect the testis each is surrounded by thick ECM which is called the tunica albuginea

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26
Q

XX fetus

A

Germ cells in gonad are organized in clusters surrounded by pre-granulosa cells
Germ cells enter meiosis
When XX is birthed, the pre-granulosa cells all degenerate only leaving the ones at the cortex of the gonad left
Each germ cell is surrounded by pre-granulosa cells
Germ cells will become oocytes
pre-granulosa cells will become granulosa cells. The rest of the mesenchymal cells will become thecal cells which forms follicles with granulosa cells.
The follicles envelop the oocyte and secrete steroid hormones such as estrogens and during pregnancy progesterone.

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27
Q

Germ cells and somatic cells of gonad

A

Germ cells are biopotential but are told what to do when they are in either male or female sex chords
They are told to begin mitosis and become eggs or arrest in mitosis and become spermatogonia (sperm stem cells)

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28
Q

Importance of germ cells in XX and XY

A

XX: the follicle cells would degenerate without germ cells
XY: The germ cells help support the differentiation of Sertoli cells but are not required for the maintenance of testis structure

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29
Q

Steps of spermogenesis

A
  1. Proliferative phase where sperm stem cells spermatogonia increase by mitosis
  2. Meiotic phase involves two divisions to create a haploid state
  3. postmeiotic phase called spermiogenesis during which round cells (spermatids) eject most of their cytoplasm and become the streamlines sperm
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30
Q

Proliferative phase of spermogenesis

A

PGCs arrive at genital ridge
Gonocytes are in sex chords that will be seminiferous tubules
Gonocytes become undifferentiated spermatogonia near the basal end of the tubular cells. Are then true stem cells
Spermatogonia reside in stem cell niches at the junction of Sertoli cells, the Leydig cells and the testicular blood vessels
Adhesion molecules join the spermatogonia directly to the Sertoli cells which will nourish the developing sperm

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31
Q

Mitotic proliferation of stem cells in XY

A

Produces type A spermatogonia which is held together by fragile cytoplasmic bridges
Glial derived neurotrophic factor (GDNF) which is secreted from Sertoli cells keeps the stem cells in mitosis
BMPs and Wnts can induce type A spermatogonia to differentiate into further sperm

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32
Q

Developmental process of sperm

A

Undifferentiated spermatogonia goes through differentiation to make differentiating spermatogonia. These cells initiate meiosis which makes spermocytes which undergo second meiosis. Then the cells undergo spermiogenesis to become spermatids

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33
Q

Type B spermatogonia

A

precursors of the spermocytes and contain high levels of Stra8

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34
Q

Spermocytes

A

last cells to undergo mitosis and divide out to generate primary spermatocytes which enter meiosis

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35
Q

primary spermatocytes

A

Undergoes meiotic division to male a pair of haploid secondary spermatocytes which complete the second division of meiosis

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36
Q

Spermatids

A

Formed after secondary spermatocytes complete a second division of meiosis
Are connected together by cytoplasmic bridges
Are haploid cells but since they are connected together they can diffuse into the cytoplasm of their neighbors and function as a diploid
As the divisions happen the cells go from the seminiferous tubule to its lumen

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37
Q

Oogenic meiosis

A

Primary oocyte goes through unequal cytokinesis after telophase I to generate second degree oocyte and a polar body

The secondary oocyte goes through another unequal cytokinesis after telophase II which gives mature ovum (egg) and another (2nd) polar body

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37
Q

Oogenesis

A
  1. PGCs (gonocytes) proliferate to make oogonia before birth
  2. In gentile ridge, oogonia associate with somatic cells to form follicles. One forms one follicle
  3. Surviving oogonia in a follicle enter meiosis I before birth. Become primary oocytes
  4. Primary oocytes pause in diplotene of prophase I
  5. Resumed at sexual maturity. ~12-40 years will be resumed meiosis in response to luteinizing hormone (LH) who is co-secreted along with follicle-stimulating hormone by the gonadotrophin cells in the adenohypophysis (anterior pituitary).
  6. Meiosis pauses again at meiosis II until fertilization
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38
Q

Dictyate resting phase

A

Meiosis arrested at first meiotic prophase and reinitiated in a smaller population of cells
Resumes during puberty

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39
Q

Retinoic acid (RA)

A

Determines timing of meiosis and sexual differentiation of mammalian germ cells

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40
Q

How Retinoic acid (RA) affects XX

A

RA activates Stra8 which is a txn factor what causes initiation of meiosis
After meiosis female germ cell fate/female differentiation occurs in the gentile ridge

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41
Q

How Retinoic acid (RA) affects XY

A

Cyp26b1 causes degradation of an acid which causes RA to not work
Nanos (late) degrades Stra8
These two factors causes meiosis to not occur which causes male fate and delayed meiosis

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42
Q

Fertilization goals

A
  1. Sexual reproduction. Genetic information from parents to offspring
  2. Initiate the development of the egg metabolism (maturation)
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43
Q

What happens during fertilization?

A

Sperm and egg contact and recognition
Regulation of sperm entry
Fusion of genetic material
Activation of the egg metabolism

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44
Q

Anatomy of sperm

A

From flagella to acrosomal vesicle:
Axoneme (made of tubulin and mitochondria), Mitochondria, Centriole, Nucleus (haploid), Cell membrane, Acrosomal vesicle (derived from Golgi; contains digestive enzymes)

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45
Q

Egg (ovum) Anatomy

A

Female pronucleus, Plasms membrane, vitelline envelope (outer jelly layer which is ECM around the egg; is important for sperm and egg recognition. Called Zona Pellucida in mammals), Jelly coat

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46
Q

What will ovulated eggs have before fertilization?

A

Cumulus, polar body, ovum and zona pellucida

47
Q

Spermatogenesis

A

Happens when organism reaches maturity
Long flagellum develops
Mitochondria accumulated to power the swimming
Nucleus condenses
Cytoplasm is released
Acrosomal vesicle forms

48
Q

Vitelline envelope, Zona Pellucida

A

ECM surrounds the egg
Composed of glycoproteins
Important for sperm/egg recognition

49
Q

Recognition of egg and sperm

A
  1. Chemoattraction of the sperm is attracted to the egg. Due to soluble molecules secreted by the egg
  2. Binding of the sperm to the ECM (zona pellucida) of the egg
  3. Exocytosis of the sperm acrosomal vesicle and release of its enzymes
  4. Passage of the sperm through the ECM to the egg cell membrane
  5. Fusion of the egg and sperm cell membranes
50
Q

What happens after the egg and sperm recognize each other?

A

The haploid sperm and egg nuclei can meet and the reactions that initiate development can begin

51
Q

Sperm translocation (mammalian)

A
  1. Sperm motility- Use flagella
  2. Sperm rheotaxis- movement in response to current. Environment works against them because the outward flow comes down fallopian tube to allow the egg to leave the tube to get into the uterus. Sperm responds to this directional cues and orients itself against outward flow
  3. Uterine muscle contractions help the sperm move to its destination
52
Q

Where do egg and sperm mostly meet?

A

In the ampulla of the fallopian tubes.

53
Q

The acrosome reaction

A

When sperm and egg meet
Sperm binds zona pellucida (ZP) proteins. ZP2 responsible for human sperm to bind to oocytes. ZP2 binds bindin.
1. The acrosomal membrane fuses with eggs membrane.
2. enzymes from inside sperm membrane are released to reveal bindin. Bindin is an egg binding protein
Are species specific polysaccharides in the egg jelly that bind receptors on the sperm membrane. Acrosomal membrane fuses and contents are released to reveal bindin.

54
Q

What happens after sperm-egg binding?

A

Izumo protein is displayed on sperm membrane
Izumo binds to Juno/CD9 protein on egg membrane -> Initiates membrane fusion of the two sperm and initiates sperm entry

55
Q

How is sperm entry regulated? How to prevent polyspermy?

A

Fast block and Slow block

56
Q

Polyspermy

A

Entry of more than one sperm
Ex. Fert. by 2 sperm = 3x DNA = triploid nucleus 3N = get multiple mitotic spindles
Each sperm brings one centriole = after duplication is 4 centrioles
With two mitotic spindles, cell tries to divide 3N genetic material into 4 cells

57
Q

Fast block (Urchins, frogs and amphibians; not mammals)

A

Change in electrical potential inside the oocyte. Immediately after sperm entry. Sperm will not want to bind to a positive membrane potential of the egg
Egg is 70 mV which is -70 mV because the inside of the egg is negatively charged in relation to the exterior
Chemicals from the fusing sperm cytoplasm alter the sodium ion channels.
Within 1-3 seconds after binding the membrane potential shifts to a positive one of +20 mV and therefore the sperm will not fuse to a positive membrane potential.

58
Q

Slow Block

A

aka cortical granule reaction (urchins and most mammals)
Mechanical removal of sperm
Enzymes are released by cortical granules and modify (cut off) ZP proteins. Enzymes are released when sperm binds egg. They are released between the cell membrane and the fibrous mat of vitelline envelope proteins. Enzyme called cortical granule serine protease.
Egg proteins (membrane receptors. Juno/CD9) are cut off as well
Therefore sperm no longer binds
Happens about one minute after sperm-egg fusion

59
Q

What elevates the fertilization envelope from the cell during slow block?

A

glycosaminoglycans which are released by cortical granules
They absorb water to make more space between the cell membrane and the fertilization envelope

60
Q

How is the fertilization envelope stabilized during slow block?

A

Crosslinking adjacent proteins through egg-specific peroxidase enzymes and a transglutaminase released from the cortical granules
This crosslinking allows resistance of shear forces of the oceans waves
As this is happening a fourth set of cortical granule proteins, including hyalin, forms a coating around the egg. The egg then extends elongated microvilli whose tips attach to the hyaline layer, which provides support for the blastomeres during cleavage

61
Q

What activates cortical granule reaction?

A

Calcium ions
Upon fertilization the [Ca2+] increases
Cortical granule membranes fuse with egg cell membrane, releasing its contents. Starts at point of sperm entry.
A wave of cortical granules exocytosis goes around the entire egg to the other side
Rise in Ca2+ is which causes cortical granule reaction is not from the rise in Ca2+ but from the endoplasmic reticulum of the egg

62
Q

What happens as cortical granules undergo exocytosis?

A

They release cortical granule serine protease (CGSP) which cleaves proteins linking to the vitelline envelope to the CM
Glycosaminoglycans form osmotic gradient, making space between the vitelline envelope and the CM
Enzyme Udx1 catalyzes formation of hydrogen peroxide (H2O2) which is a substrate for soluble ovoperoxidase (OVOP). OVOP and transglutaminases (TG) harden the vitelline envelope, now called the fertilization envelope

63
Q

What happens after the egg is activated?

A

Effects of cytoplasmic calcium wave:
-Causes it to finish meiosis II (urchins already did meiosis II)
- Cortical granule release
- Translating maternal mRNA
Glucose is used to give energy for biosynthesis
TCA produces ATP + NADH + FADH –> e- carriers needed for metabolic rxns

64
Q

Events of/after fertilization (Early Events, 1st minute)

A

Sperm-egg binding
Fertilization potential rise (fast block to polyspermy)
Sper-egg membrane fusion
Calcium increase first detected
Cortical granule exocytosis (slow block to polyspermy)

65
Q

Events of/after fertilization (Late Events, 1-5 minutes later)

A

Activation of NAD kinase
Increase in NADP+ and NADPH
Increase in O2 consumption
Sperm entry
Acid efflux
Increased in pH (remains high)

66
Q

Events of/after fertilization (Later Events, from 5 minutes after until the first cell division)

A

Sperm chromatin decondensation
Sperm nucleus migration to egg center
Egg nucleus migration to sperm nucleus
Activation of protein synthesis
Activation of amino acid transport
Initiation of DNA synthesis (replication and txn occurs)
Mitosis and cytokinesis
First cleavage

67
Q

What happens after cytoplasmic Ca2+ wave?

A

Resumption of meiosis (except in urchins and cnidarians
Cortical granule release
NAD Kinase activation

68
Q

How does metabolism work?

A

Glucose –glycolysis–> pyruvate –oxygen–> oxidative phosphorylation in mitochondrion to make ATP
Therefore with energy you get biosynthesis

69
Q

What does the NAD kinase do after it is activated by Ca2+ release?

A

Converts NAD+ to NADp+ + NADP

70
Q

What does Calcium release do?

A

Activation of NADK for lipid biosynthesis. From NAD+ to NADp+ and NADPH

Causes cortical granule exocytosis which causes slow block to polyspermy

71
Q

Sperm nucleus entry (1-5 min)

A

Sperm nucleus enters the egg cytoplasm
pH increase in egg cytoplasm
Oocyte molecules decondense the sperm chromatin (release protamine’s) There will be no transcription from sperm DNA if you do not do this
Egg and sperm pronuclei migrate toward one another
Activation of protien-synthesis. Not from newly made genetic material, but material already in the cell (maternal mRNA in egg before fert.)

72
Q

Maternally contributed mRNAs

A

Histones
Cytoskeleton proteins
Cell cycle regulators
Transcription factors
Body patterning proteins

73
Q

Translational regulation in oocytes (“unmasking”)

A

mRNA gets masked so they don’t get degraded
1. BEFORE FERTILIZATION!!!! Maskin (inhibitory effect) links 5’ cap and 3’ cap end (via protein cytoplasmic polyadenylation element binding protein (CPEB)) at the short end of the poly A tail of mRNA in a repressive loop
2. FERTILIZATION!!!!! (or ovulation) activates a kinase that P’s CPEB to cause a change in CPEB shape which allows it to bind to other 3’ UTR binding proteins
3. Maskin is displaced and translation occurs

74
Q

Ways to see if transcription has occurred after fertilization

A

Three radioactive tracers!!
Thymidine –> Can see if new DNA is being formed
Uracil –> Can see if new RNA is being transcribed
Sulfur/A.A. –> Can see if new protein is being made

75
Q

What does actinomycin do the sea urchin zygotes?

A

It is an inhibitor and inhibits txn.
Initial burst of translation is from maternal mRNAs

76
Q

Cleavage

A

Period of rapid (not rapid in mammals) cell division up until “mid-blastula transition” (MBT)

77
Q

Goals of cleavage

A

Increase in number of cells
Make smaller cells for organism
decrease cell size

78
Q

How can it be achieved to decrease cell size during cleavage?

A

Reduce or skip G1 and G2 phases
Faster than normal S phase/DNA rep.

79
Q

How does the cell reduce or skip G1 and G2 phases?

A

Produce mitosis-promoting factor (MPF) which is made of cyclin B and cyclin dependent kinase (CDK)
Cyclin expression oscillates and cells enter mitosis when levels are high

During first cleavage MPF is regulated by maternal cytoplasmic factors such that it is constantly being made which leads to faster cell cycles/mitosies

80
Q

How does the cell get faster S phase/DNA replication during cleavage?

A

More origins of replication than normal
More DNA pol. made

81
Q

Maternal gene transcription

A

During diplotene (mammals pause 1st time), maternal RNAs are transcribed but not translated
When meiosis resumes, germinal vesicle breaks down, maternal RNAs enter cytoplasm. Maternal RNAs get distributed to different cells and not all get translated. Start to establish different differentiation

82
Q

What happens in early development

A

Rapid synchronous cleavage
maternal mRNAs are deposited into different cells
activated maternal affect genes

83
Q

Mid-Blastula transition (MBT)

A

maternal mRNAs are depleted
rate of mitosis slows down
activation of zygotic gene transcription
cellularization (in drosophila)

84
Q

What happens to form the cellular blastoderm?

A

syncytium –> syncytium blastoderm –> cellular blastoderm
Nuclear elongation –> cellularization
occurs after cycle 13
coordinated by cytoskeleton (actin, myosin and microtubules)

85
Q

syncytium blastoderm

A

all the cleavage nuclei are contained within a common cytoplasm. No cell membranes exist other than that of the egg itself.

86
Q

Role of actin and myosin in blastoderm formation

A

pulls in membrane to pinch it off like cytokinesis

87
Q

What does gastrulation lead to?

A

Segmentation
Anterior vs. Posterior

88
Q

A/P axis during oogenesis

A

progressive developing structures/follicle
progressive movement goes top to bottom with bottom being more developed (at the oviduct) Top of ovariole is less developed

89
Q

How is A/P polarity established in the oocyte?

A

Gurken is transcribed in nurse cells
Gurken mRNA is moved to oocyte and translated
At positive end of egg chamber, gurken signal binds to torpedo receptors on posterior of follicle cells (become posterior end where follicles are)
Posterior follicle cells send a singla back to oocyte which activates protein kinase A which recruits Par-1 protein to posterior edge of oocyte cytoplasm
Par-1 organizes MTs in a specific way with their negative ends toward anterior and positive ends (growing ends) towards the posterior
Positive end motor kinesin transports Osker (nanos is associated with this protein) protein (recruits more Par-1) to the posterior
Negative end dynein transports bicoid to the anterior of the oocyte

90
Q

Maternal effect genes and A/P pattern formation

A

mRNAs placed in different regions of the syncytial egg cytoplasm –> they will regulate transcription and translation of zygote genes which will establish A/P and help divide embryo into segments

91
Q

Specifying identity steps in flies

A

specification- gradients of maternal effect proteins
determination- established by formation of segments
Differentiation
All is controlled by segmentation genes

92
Q

A/P pattern formation steps

A

Maternal affect genes to establish A/P polarity
Activate GAP genes (txn factors)
Activates Pair-Rule genes (txn factors)
Activates segment-polarity genes (Not txn factors. Are signal molecules) Are determined at their point b/c segments are established
Homeotic genes (txn factors) going to control fate of segment

93
Q

bicoid is located where?

A

The anterior, negative side
head side

94
Q

nanos is located where?

A

The posterior, positive side
tail side

95
Q

What do the protein gradients regarding A/P pattern formation?

A

gradients of proteins acts a morphogen
concentration dependent
Establish by diffusion of proteins

96
Q

What happens in bicoid loss of function mutants?

A

No head structure is formed, two sets of tails is formed

97
Q

What happens in bicoid misexpression mutants?

A

New head regions/ new anterior regions in a concentration dependent manner

98
Q

Can Bicoid and Nanos regulate other maternal mRNAs?

A

Yes!
caudal mRNA translation is inhibited by expression of bicoid
hunchback mRNA translation is inhibited by expression of nanos protein

99
Q

Four maternal proteins of developing drosophila

A

Nanos- helps with embryos development. Translation inhibitor through RNA binding
Bicoid, Hunchback, and Caudal are transcription factors regulate zygotic gene transcription

100
Q

Gap genes (example)

A

transcription factor, expression pattern determined by maternal proteins and repressive interactions with other gap gene proteins

Ex’s.
Kruppel
Mutant would miss large region of body resulting in a gap

Hunchback and Knirps

Kruppel and Giant inhibit each others expression. Makes mountains in a graph where ones peak is the others rock bottom then they swap

101
Q

Love triangle of bicoid, hunchback and knirps

A

Caudal causes knirps
Bicoid activates both hunchback and knirps
Hunchback inhibits knirps
Knirps inhibits hunchback
Hunchback is victor of the inhibition

102
Q

Pair-rule genes (transcription factors)

A

pair of them are expressed in non-overlapping segments
Each expressed as seven evenly spaced strips
Stripes of complementary genes are non-overlapping

103
Q

What happens in Pair-rule gene loss of function mutants?

A

Mutant lacks portions of each segment

104
Q

How do Cis elements affect pair-rule expression?

A

They control pair-rule expression
Non coding sequences that control when/where/how much of a gene is transcribed

105
Q

Enhancer and repressor sites for eve stripe 2?

A

Bicoid; Caudal; Giant; Hunchback; Kruppel; Knirps; Tailless
Gap genes are turning on/off pair-rule genes in a very precise way which is how we get pair-rule pattern(s)

106
Q

The segment polarity genes

A

engrailed is expressed in posterior compartment of each segment
Wingless (Wnt) is in anterior compartment of each segment

107
Q

Pair-rule –> segment polarity

A

Wingless is expressed in the intervening spaces during lack of Eve and Ftz
Engrailed is in cells with high concentrations of Eve or Ftz

108
Q

Segment polarity genes

A

segment polarity genes are signaling centers that create gradients of morphogen
Ex. wg and Hh

108
Q

Hedgehog and wnt expression feedback loop and its positives

A

We get a loop which is beneficial because they are not expressed forever then they fade away
wg. is expressed which causes wnt paracrine factor which binds to frizzled receptor on neighboring cell
The wnt factor allows Beta-catenin to not be degraded so it can go to the nucleus and changes gene expression which activates engrailed expression
This txn factor activates hedgehog expression which leaves the cell and goes to the first cell in the loop which has hedgehog receptors.
The hedgehog receptor takes the factor and causes wg expression which causes wnt expression and the cycle repeats

109
Q

Homeotic selector genes

A

aka Hox genes!
Genes specify structures on segments
Cluster of genes that function like a single unit
Location/position on the chromosome is linked to location of expression in the animal

110
Q

Homeotic mutant examples

A
  1. Ubx mutant allows the Antp to expand in its domain to get another set of wings in the place of Ubx place
    Fly gets two second thoracic segments instead of one
  2. Gof mutant allows the Antp domain to grow where the antennas would be
    The result is a pair of legs where the antennas would be
111
Q

Paralogues

A

Same gene in organism

112
Q

Why are there four “Hox” complexes in mice

A

Results from gene duplication during mouse evolution

113
Q

What is the Hox hypothesis?

A

Means combinations of these gene’s expressions specify fate of regions along the A/P axis

114
Q

Evidence for the Hox Code hypothesis?

A

Comparative anatomy- Compare types of vertebrate cross vertebrate species. Differences in Hox expression boundaries correlate with differences in skeletal structure

Knockout of KO expression. Complete knockout of Hox 10 (a,c,d) resulted in the expansion of the thoracic region and the sacral as well. Lumbar converted to thoracic vertebrate. Hox 10 –> Hox 9 fate

Complete knockout of Hox 11 (a,c,d) resulted in sacral vertebrae are lost and are lumbar vertebrae. Extension of Hox 10 domain.