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ACB- Development > Pre-Midterm > Flashcards

Pre-Midterm Flashcards

1
Q

What is developmental biology?

A

the study of the changes in the anatomical form (morphology) and physiology of an organism as it progresses through the various stages of its life cycle, and of the intricately coordinated changed in cell and gene activities that control those transitions

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2
Q

What are the different developmental stages?

A 
gametogenesis
fertilization
cleavage
gastrulation
organogenesis
metamorphosis
Maturation and aging
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3
Q

Define teratology?

A

congenital birth defects and their causes

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4
Q

What occurs in gametogenesis and fertilization?

A

the sperm and ovum to become a zygote

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5
Q

What occurs in embryonic development?

A

zygote to hatching and birth

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6
Q

What is “Evo-Devo”?

A

evolutionary developmental biology

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7
Q

What occurs in metamorphosis?

A

a larva becomes an adult

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8
Q

What occurs in maturation and aging?

A

juvenile to an adult to senescence

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9
Q

What occurs in regeneration?

A

organ repair and replacement

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10
Q

What are different developmental processes?

A

cell proliferation and tissue growth, apoptosis, cell migration vs. cell adhesion, cell-cell signalling, cell fate specification and cell differentiation, determination of body axes and pattern formation, morphogenesis and organogenesis

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11
Q

What did Roux conclude in his experiments?

A

each blastomere received only half of the genetic information of the fertilized egg

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12
Q

What experiment did Roux conduct?

A

used a 2 blastomere frog embryo, destroyed 1 blastomere with a hot needle and found that only one embryo developed

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13
Q

What flaw was in Roux’s design?

A

when he destroyed one blastomere he left them in contact with the other which got in the way with the differentiation of the intact blastomere

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14
Q

What experiments did Driesch conduct?

A

took a 4 cell sea urchin and separated the 4 blastomeres and found that four complete embryos developed

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15
Q

What conclusions did Driesch come to?

A

each blastomere is “totipotent” meaning it is able to form an entire embryo. each nucleus of each blastomere contains the complete genetic information required to form all cell types and tissues of the embryo

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16
Q

How many blastomeres compose a morula?

A

16

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17
Q

What experiments did Spemann conduct?

A

took a fertilized salamander egg and put a constriction on the dividing nuclei to one half of the cytoplasm, then at the 16 cell stage let one nucleus through and found the uncleared egg to begin to divide and two complete tadpoles developed

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18
Q

What was the conclusion of Spemann’s experiments?

A

each nucleus retains all genetic information and remains totipotent, at least until the 16 cell stage

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19
Q

What experiments did Briggs and King conduct?

A

at the blastula stage they removed a single blastomere cell, removed its nucleus and then inject the blastomere nucleus into an enucleated egg

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20
Q

What is an enucleated egg?

A

an unfertilized egg that has had its nucleus removed

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21
Q

What were the conclusions of the experiments by Briggs and King?

A

cells at the blastula stage remained totipotent

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22
Q

Do cells remain totipotent in gastrulation?

A

at this stage the cells move around and form the three germ layers, the success of development in an enucleated egg declined as passes through gastrulaiotn

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23
Q

What is SCNT?

A

somatic cell nuclear transfer

- taking a nuclei and placing it into the enucleated cell

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24
Q

What experiments did Gurdon conduct?

A

he demonstrated that there is not selective gene elimination because he showed that nuclei isolated from cells of organogenesis and later in cell life could form a complete animal when in an enucleated cell

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25
Q

What experiment did Wilmut conduct?

A

he did the first successful clone of a mammal “dolly”

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26
Q

Will genetic clones have identical phenotypes?

A

not necessarily, a phenotype is influenced by the genes, environmental factors and epigenetic modifications to chromatin, and randomized processes in development (such as the silencing of an X chromosomes in female)

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27
Q

What did Yamanaka’s experiments do?

A

he demonstrated that fibroblast cells from the skin of adult mice and humans could be reprogrammed back into an undifferentiated, pluripotent state by infection with a virus expressing the pluripotwncy genes

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28
Q

What are the pluripotent genes?

A 
Oct4
Sox2
Klf4
c-Myc
Nanog
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29
Q

What are iPS cells?

A

induced pluripotent cells- they have the ability to forma variety of distinct, differentiated somatic cells

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30
Q

Define: Pluripotent

A

their mitotic progeny form all differentiated somatic cell types of the body during normal embryonic development

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31
Q

What is the difference between totipotent and pluripotent?

A

toti- have the ability to be anything, including the placenta and embryo
pluri- can become any cell of the body

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32
Q

Define: differential gene expression

A

the genes remain the entire set of genes but selectively transcribes and translates based on the cell type

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33
Q

What are housekeeping genes?

A

expressed by all or most somatic cell types

- provide proteins for basic cell structure and metabolism

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34
Q

What are tissue-specific genes?

A

genes that are expressed by only certain cell types

- a cell’s phenotype is determined by the particular group of tissue-specific genes that is expressed

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35
Q

What is the principle of genomic equivalence?

A

in general, the somatic (all-but-gamete) cells of an organism retain all of their genes throughout development

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36
Q

How is there cell diversity even though they retain all of the information?

A

through differential gene expression. the same group of genes, expressed in different combinations, can direct the differentiation of many distinct cell types

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37
Q

At what end of genes can there be addition of more info?

A

at the 3’

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38
Q

What way are genes read?

A

5’ to 3’

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39
Q

What is a promoter?

A

at the 5’ end of a gene just before the transcription start site. it is where RNA polymerase 2 binds and begins to create mRNA at the transcription start site

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40
Q

In what order is the functional RNA made in?

A

5’ to 3’, because 3’ is preferable to add to so the template is made off of the 3’ to 5’ strand of DNA

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41
Q

What end of DNA is preferable for adding nucleotides?

A

the 3’ end

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42
Q

What free group is at the 5’ end?

A

phosphide

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43
Q

What free group is at the 3’ end?

A

hydroxide

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44
Q

What is the transcription termination site?

A

RNA polymerase 2 continues making mRNA until it reaches the transcription termination site, then it dissociates from the DNA template

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45
Q

What different processes occur to the pre-mRNA?

A

5’ methyl guanosine cap
3’ poly A tail
splicing

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46
Q

What is the purpose of the 7-methylguanosine cap?

A

addition to the 5’ end allows the processed mRNA that exits the nucleus to bind the ribosomes and get translates
- may also protect from degradation by exonucleases

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47
Q

What is the purpose of the poly-A tail?

A

helps to protect the 3’ end of the mRNA transcript from degradation by exonuclease, and probably facilitates its attachment to ribosomes

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48
Q

What are introns?

A

regions of the RNA that are not included in the mature RNA

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49
Q

What are exons?

A

the portions of pre-RNA that remains intact to become mature mRNA

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50
Q

What is splicing?

A

the removal of introns and ligation of axons to allow for uninterrupted protein coding domain within the mature mRNA

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51
Q

What is the UTR?

A

the untranslated regions at the 5’ and 3’ ends of mature mRNA

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52
Q

How is differential expression displayed through transcription?

A

a gene may be actively transcribed into RNA or may be transcriptionally inactive

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53
Q

How is differential expression displayed through processing?

A

the nuclear pre-mRNA transcript must be properly processed to for functional mRNA

  • 7methylguanosine cap
  • poly a tail
  • removal of introns and splicing axons together (can have alternative splicing here)
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54
Q

What is alternative splicing?

A

can yield different mRNA from the same pre-mRNA through a different combination of exons
- allows it to code for multiple protein products

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55
Q

How can differential gene expression occur at the level of RNA stability and turnover?

A

the longevity of mRNA transcripts can differ

- if newly formed mRNA transcript is rapidly degraded, it can not bind ribosomes and form a protein product

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56
Q

Wha is miRNA?

A

microRNA and they are small non-coding RNA that attach to specific mRNA in cytoplasm and either inhibit their translation or selectively target them for degradation

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57
Q

How is differential gene expression displayed at the level of translation?

A

mRNA may be prevented from binding to ribosomes and being translated into a polypeptide

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58
Q

How is differential gene expression displayed at the level of post-translational modifications?

A

to forma functional protein, the polypeptide must be properly folded

  • different modifications can affect folding ability
  • proteolytic processing affects tissue-specific functions
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59
Q

What are common post-translational modifications?

A 
prenylaiton
disulfide bonds
hydroxylation
sulfation
methylation
phosphorylation
glycosylaiton
acyl lipidation
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60
Q

How do post-translational modifications affect a peptide?

A

they affect the protein folding, but also protein localization, binding partners, and stability

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61
Q

At what levels is there differential gene expression?

A 
transcription
processing
RNA stability and turnover
translation
post-translational modifications
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62
Q

What are transcription factors?

A

proteins that bind to specific nucleotide sequences in a gene’s promoter or to other regulatory sequences (enhancers and silencers) to control levels of gene transcription

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63
Q

What are activator transcription factors?

A

stimulate transcription of their target genes

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64
Q

What are repressor transcription factors?

A

suppress transcription of their target genes

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65
Q

What are general transcription factors?

A

they are present in most cell types

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66
Q

What are tissue-specific transcription factors?

A

they are selectively present in only certain cell types, at specific anatomical sites, or at specific time points in development

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67
Q

What is a promoter?

A

a regulatory element of the gene located within 200 bp upstream (5’) of the transcription start site
- contains the basal promoter sequences and serve as a docking site for general transcription factors where binding is required to recruit RNA polymerase 2 to the gene’s transcription start site

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68
Q

What are common promoter regions?

A

TATA box
CAAT box
GC box

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69
Q

What is the first protein to bind to the TATA/Inr basal promoter sequence?

A

TBP which is a subunit of the TFllD complex

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70
Q

What is the sequential assembly of general transcription factors?

A

TF2D complex
TF2A
TF2H
- then can recruit, and phosphorylate to activate RNA polymerase 2 so it is more likely to form the template

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71
Q

Do the basal promoter sequences play a role in differential gene expression?

A

no

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72
Q

Do the general transcription factors play a role in differential gene expression?

A

no

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73
Q

What are enhancers?

A

regulatory nucleotide sequences of 50-1000bp that can be located anywhere within the same chromosome (5’, 3’ or within an intron)
- serve as docking sites for tissue-specific or stage-specific transcription factors. which are activator transcription factors that are present only in some various cell types of the body

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74
Q

What binds to enhancers?

A

tissue-specific or stage-specific transcription factors

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75
Q

What occurs when a tissue-specific transcription factor binds to an enhancer?

A

it helps to activate the gene’s promoter and increases the efficiency of the gene’s transcription to physiologically relevant levels

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76
Q

Is an enhancer is far away, how will it get closer to a promoter?

A

DNA bending and mediator proteins bring together enhancers and promoters
- brings together

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77
Q

Where is Pax6 located?

A

it is a transcription factor present only in the nuclei of cells in developing eyes (lens, cornea, and retina), pancreas, and neural tube
- crucial for eye formation

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78
Q

Does having a specific transcription factor mean a gene is expressed?

A

no, they must act in combination with other transcription factors for cell-specific gene activation

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79
Q

What transcription factors are required for expression of the crystallin gene?

A

in lens cells, Pax6 works together with Sox2, Man, and deltaEF3 transcription factors to activate transcription

80
Q

What transcription factors are required for expression of the somatostatin gene?

A

in pancreatic cells, pax6 works with Pbx1, Pdx1, and CREB transcription factors to activate transcription

81
Q

What are silencers?

A

regulatory sequences that suppress the gene’s transcription in inappropriate times of development

  • act as binding sites for repressor transcription factors
  • experimental deletion of a gene’s silencer sequence increases its level of transcription
82
Q

What is a NRSE silencer element?

A

found in several neural-specific genes and blocks expression of these genes in non-neural tissues of mouse embryo

83
Q

Why is there differential gene expression?

A

to generate cel type diversity

84
Q

What is chromatin?

A

histones and the genome

- condensed chromatin limits transcription

85
Q

What is chromatin remodelling?

A

histone protein acetylation and methylation can influence transcription

86
Q

What occurs if there is DNA methylation in the gene’s promoter?

A

represses transcription
genomic imprinting
also for X chromosome inacitvation

87
Q

What is the purpose of histones?

A

help to give gem one structure

- the DNA helix is wrapped around clusters of positively charged histone proteins to form nucleosomes

88
Q

What comprises the nucleosome core>

A

histone octamer (H2A, H2B, H3, H4)x2

89
Q

How many loops of DNA wrap around each nucleosome core?

A

2 loops of DNA

and 60bp of linker DNA separate nucleosomes

90
Q

Purpose of H1?

A

draws nucleosomes together into compact clusters

- interact to form a superstructure

91
Q

How do histones regulate gene accessibility?

A

tight packing of genes in nucleosomes clusters resiricts their accessibility to transcription factors and RNA polymerase
- local chromatin relaxation is requires to expose the gene’s promoter and enhancer sites to increase accessibility to transcription factors and RNA polymerase

92
Q

How does acetylation affect DNA and histone binding?

A

negatively charged DNA is attracted to positively charges lysine on H3 and H4 tails
- with acetylation of the H3 and H4 tails it neutralizes the charge and weakens the attraction

93
Q

HAT

A

histone acetyl transferase

- increases accessibility

94
Q

HDAC

A

histone deacetylases

- decrease accessibility

95
Q

What does TAF250 do?

A

it is a subunit of the TFIID general transcription factor complex and it functions as a histone acetyltransferase
- meaning it can acetylate and displace a nucleosome from a promoter

96
Q

What does p300/CBP do?

A

transcriptional co-activator proteins that interact with a variety of different transcription factors and recruit the histone acetyltransferase P/CAF

97
Q

What are pioneer transcription factors?

A

they can access even tightly packed chromatin to initiate local chromatin relaxation

98
Q

What is an example of a pioneer transcription factor?

A

Pbx1

99
Q

What areas of chromatin can be methylated?

A

lysine or arginines on histone tails can be methylated by proteins such as histone methyltransferases

100
Q

How does histone methylation alter gene accessibility?

A

can repress or promote transcription depending on which specific lysine in the histone tail are methylated and how many methyl groups are present on each site

101
Q

What is a common methylation site?

A

in vertebrate DN, many cytosine bases occurring in CpG pairs are methylated

102
Q

What is a CpG sequences?

A

successive bases along one DNA strand, distinguishing from CG which often refers to base pairing across DNA DNA strands

103
Q

What catalyzes DNA methylation?

A

DnMt’s

DNA methyl transferase

104
Q

What is the effect of DNA methylation in a gene’s promoter?

A

repression of transcription

methylated promoted = not expressed

105
Q

What is an example of stage-specific differential gene expression utilizing methylation of a promoter?

A

the switch from embryonic globin to fetal gamma globin synthesis during fetal blood cell maturation is accompanied by increased methylation of the embryonic gene promoter and demethylaiton of the fetal gene promoter

106
Q

How does DNA methylation of the promoter affect histone methylation?

A

methylated cytosine sin a gene may attract MeCP2 protein, which recruits HDACs to deacelyate adjacent histones and cause local chromatin condensation (which represses transcription)

107
Q

How does histone methylation affect DNA methylation?

A

tri-methylation of lysine 9 of histone H3 can repress transcription by attracting DNA methyltransferase (Dnmt) which causes methylation of CpG sites on adjacent DNA to decrease gene transcription

108
Q

How is a pattern of DNA methylation inherited during cell division?

A

in vertebrates, gene methylation is an important mechanism for stabilizing the repressed state of transcriptionally inactive genes as differentiated somatic cells undergo multiple cycles of mitotic division

109
Q

What is genomic imprinting?

A

related to the idea that the pattern of DNA methylation is inherited during cell division
- certain genes are only transcriptionally active when located on a paternally or maternally derived chromosome

110
Q

When does genomic imprinting occur?

A

during gametogenesis as a consequence of differences in cytosine methylation of critical control regions of the imprinted genes during sperm vs. egg formaiton

111
Q

DMR

A

differentially methylated region

112
Q

What is an insulator protein?

A

CTF

- binds to unmethylated DMR sequences

113
Q

How is Igf2 influenced by genomic imprinting?

A

on the maternal chromosome an enhancer drives H19 transcription if insulator protein CTF is on the DMR and no Igf2 transcription.
on paternal methylation blocks H19 transcription so the enhancer drives Igf2 transcription

114
Q

What is the outcomes of a deletion mutation of the paternal copy of Igf2?

A

there is a dwarf size fetus

- it would normally be expresses so deletion shows an effect

115
Q

What is the outcome of a deletion mutation of the maternal copy of Igf2?

A

there is a normal size fetus

- normally not expressed due to genomic imprinting so it will not have an effect

116
Q

Where is the IGF2 Receptor expressed?

A

only the maternally derived copy of the gene for the IGF2 receptor is active

117
Q

What occurs if there is an embryonic deletion mutation of the paternal copy of Igf2r?

A

there is a normal fetus size

- the gene for the receptor is only maternally derived

118
Q

What occurs if there is an embryonic deletion mutation of the maternal copy of Igf3r?

A

there is an abnormally large fetus

- because the gene for the receptor is maternally derived

119
Q

How does the Igf2/Igf2r system work?

A

IGf2 stimulates fetal growth through other Igf receptors, whereas Igf2r prevents excessive fetal growth by targeting excess Igf2 for degradation. so growth is normal when Igf2 and Igf2r levels are balanced

120
Q

Why are male sheep buts large?

A

Genomic imprinting
CLPG gene os sheep is only active on paternal copies
- a mutation of CLPG on the active paternal copy of gene causes enlargement of rump musculature, whereas the same mutation on maternal has normal rump phenotype

121
Q

What is X chromosome inactivation?

A

usually starts in the XIC locus and spreads, mediated by Xist that inactivates either the paternally or maternally derived X chromosome so the chromatin becomes highly condensed and forms a barr body

122
Q

At what point is there X chromosome inactivation?

A

at an early stage go blastocyst development inside the inner cell mass, one of two X chromosomes will undergo inactivation.
- doe snot matter which one

123
Q

What is responsible for a patchy fur pattern of colouration on calico cats?

A

random X chromosome inactivation, because different X are inactivated early on and so it is a mosaic of different X chromosome derived cells

124
Q

Are cloned calico cats identical?

A

no, because there is differences in random X chromosome inactivation

125
Q

What are primordial germ cells?

A

diploid progenitor cells of haploid gametes

126
Q

When are pGCs formed?

A

at an early stage of embryonic development

127
Q

When are haploid gametes produced?

A

in sexually mature adults

128
Q

Where do PGCs originate?

A

outside of the embryonic gonads then migrate to the gonadal primordia

129
Q

Wunen protein

A

in drosophila, produced by the gut tissue and repels the pole cells

130
Q

Hedgehog protein

A

in drosophila, a protein secreted by developing gonads and acts as a sobuble chemotactic factor that attracts pole cells to the gonads

131
Q

What are three complimentary tests in developmental biology?

A
  1. remove a structure and see what happens
  2. put the variable back in
  3. put the variable in a different area
132
Q

What are the molecular components of the drosophila pole plasm?

A

pole plasm contains a variety of regulatory RNAs and proteins
- many act as transcriptional or translational repressors that suppress gene expression in pole cells

133
Q

Inert Genome Hypothesis

A

By repressing expression of genes required for differentiation of various somatic cell types, the pole plasm may direct the pole cells into the gamete-forming lineage

134
Q

Maternal effect mutations

A

a defective genotype in the mother results in a defective phenotype in her offspring

135
Q

Nanos

A

found in the pole plasm of drosophila, together with pumilio it binds to the 3’UTR of some mRNA and inhibits the translation

136
Q

Pole Granule Component

A

found int he drosophila pole plasm, a non-coding regulatory RNA in the pole plasm that inhibits gene transcription by inhibiting RNA polymerase 2 activation

137
Q

Piwi

A

in the pole plasm of drosophila, acts with microRNA in an “RNA silencing” complex that inhibits translation by promoting enzymatic destruction of specific mRNAs in pole cells

138
Q

Vasa

A

in the pole plasm of drosophila, an RNA binding protein that functions as a translation initiation factor, it promotes translation of mRNAs coding for proteins involved in pole cells differentiations

139
Q

Oskar

A

in the pole plasm of drosophila, it organizes and anchors other pole plasm determinants in posterior cytoplasm of the egg

140
Q

What occurs of Oskar is expressed at the anterior drosophila zygote?

A

pole cells will form ectopicaly at the anterior end

141
Q

What genes in drosophila also function in PGC formation and germ cell differentiation in vertebrate species?

A

Nanos- requires for PGC migration and survival in amphibians, fish, and mammals
Vasa- mutations disrupt spermatogenesis
Gcl- mutations disrupt spermatogenesis and reduce fertility

142
Q

In mammals, where do PGCs develop?

A

from a small cluster of cels that express both Blimp1 and Prdm14 transcription factors

143
Q

Stem Cell Factor SCF

A

a growth factor produced by cells that surround the migrating PGCs in mammals

144
Q

Steel mutation

A

mutation of gene coding for SCF in mice

145
Q

White-spotting mutation

A

mutation of the gene coding for c-kit, the receptor for SCF in mice

146
Q

Contact guidance

A

in PGC migration, in frogs and mammals PGCs move by ameboid extension of filopodia
- the oriented alignment of fibronectin fibrils along the migratory route may help guide PGCs toward gonadal ridges

147
Q

Chemotaxis

A

in some vertebrates (fish, mice, humans) the developing gonads secrete a diffusible chemotactic protein SDF-1, that attracts the PGCs (binds CXCR4 on the surface of PGCs)

148
Q

What genes maintain pluripotent in mammalian PGCs?

A

OCT4, SOX2, NANOG

149
Q

What occurs if PGCs fail to reach the gonads?

A

teratoma tumours

- typically contain a jumbled mass of diverse differentiated tissue types

150
Q

What expressed pluripotent genes?

A
  1. PGCs
  2. Inner cell Mass of mammalian blastocyst
  3. human embryonic stem cells
  4. induced pluripotent stem cells
151
Q

What are induced pluripotent stem cells?

A

cells that can be reprogrammed from adult somatic cells through transcription factors to become pluripotent

152
Q

Diapedesis

A

the passage through intact walls (ie. between the cells)

153
Q

In mammalian PGCs what determines their differentiation pathway?

A

the type of gonad that the PGCs enter (ovary or testis) determines the differentiation pathway (oogonia vs. spermatogonia)
AND it determines the time in development when oogonia and spermatogonia cells initiate meiosis

154
Q

What directs PGCs to develop into oogonia?

A

the female gonadal ridge (future ovary) produces Wnt4

155
Q

What triggers oogonia to enter meiotic prophase 1?

A

the mesospheric kidneys secrete retinoid acid which activates Stra8 expression in oogonia. Stra8 triggers the oogonia to enter meiotic prophase 1

156
Q

Describe the Wnt pathway in the absence of Wnt?

A

beta-catenin transcription factor is degraded by Axis, APC, and GSK3 in the cytoplasm

157
Q

Describe the Wnt pathway in the presence of Int?

A

Want binds to Frizzled where Dsh and Axis are intracellular and bind. the complex cannot form for beta-catenin degradation so it can go to the nucleus and activate target genes

158
Q

In humans and mammals, when do oogonia initiate meiosis?

A

during the period of embryonic development

159
Q

Describe the retinoid acid signalling pathway?

A

retinol (vitaminA) using RDH to retinal, using RALDH to retinoid acid. retinoid acid enters the cell an binds RARalphaRXR on Rare gene for the transcription of Star* gene

160
Q

What directs PGCs to develop into pre-spermatogonia?

A

the male gonadal ridge (testis primordial) produces FGF9 causing PGCs to develop into pre-spermatogonia (gonocytes)

161
Q

In spermatogonia, how is the initiation of meiosis prevented?

A

the male gonadal ridge (testis primordial) produces CYP26B1 that degrades retinoid acid which inhibits Star* expression and the low level of Star* prevents initiation of meiosis

162
Q

When is there reductional division?

A

Meiosis 1

163
Q

When is there equational division?

A

Meiosis 2

164
Q

Leptotene

A
  • chromosomes are thin and thread like

- individual sister chromatids are not yet visible

165
Q

Zygotene

A
  • homologous chromosomes pair-up (synapsis) joined by the synaptonemal complec
166
Q

Pachytene

A
  • chromosomes thicken; individual sister chromatids become visible (tetrad)
  • beginning of crossing over: genetic recombination in which segments of paired homologous chromosomes are exchanged
167
Q

Diplotene

A
  • synaptonemal complex dissolves
  • homologous chromosomes begin separating, but are still held together at chiasmata (sites of crossover)
  • typically high transcriptional activity (lampbrush chromosome stage)
168
Q

Diakinesis

A
  • nuclear membrane breaks down
  • chromosomes condense further
  • transcription ceases
169
Q

gonocytes

A

pre-spermatogonia

170
Q

What changes have to occur for spermatogenesis?

A

seminiferous tubules hollow out
tubule epithelial cells - sertoli cells
pre-spermatogonia- spermatogonia proper

171
Q

What are the two types of spermatogonium?

A

Type A: the source for spermatogonia (reserve, no active mitosis) or divide to produce type B
Type B: undergo growth and become primary spermatocytes

172
Q

GDNF

A

from sertoli cells maintains mitotic proliferation of Type A spermatogonia located adjacent to basement membrane of seminiferous tubule

173
Q

How is meiosis triggered in males?

A

at puberty retinoid acid released from sertoli cells activates Stra8 in Type B spermatogonia to trigger the onset of meiosis

174
Q

What is the lineage from spermatogonia to spermatozoa?

A

type A produce more type A and lots which will become Type b linked by cytoplasmic bridges. These are now primary spermatocytes when they will undergo meiosis 1 to be secondary spermocytes and then meiosis 2 to be spermatids. then spermiogenesis to form spermatozoa

175
Q

Why are there cytoplasmic bridges?

A

there is incomplete cytokinesis during mitotic divisions of the spermatogonia and subsequent meiotic divisions. so they develop in a syncytium joined by cytoplasmic bridges which synchronizes their divisions and differentiaiton

176
Q

Spermiogenesis

A

morphological differentiation of spermatid into a spermatozoan

177
Q

What does the golgi become in spermiogenesis?

A

the acrosomal vesicle which contains lytic enzymes

178
Q

What does the centriole become in spermiogenesis?

A

elaborates an elongated flagellum

179
Q

Where do the mitochondria aggregate in spermiogenesis?

A

at the base of the flagellum

180
Q

What occurs in the nucleus in spermiogenesis?

A

nucleosome histone are replaced by more highly positive protamines and transcription ceases

181
Q

Where are oogonia arrested before puberty?

A

before birth mammalian oogonia are arrested in diplotene of prophase 1

182
Q

What influences the development of oogonia?

A

at puberty, during each menstrual cycle clusters of primary oocytes periodically resume growth under the influence of FSH and LH from the pituitary
- accompanied with mitotic proliferation of surrounding ovarian follicle cells )granulose cells)

183
Q

What triggers the resumption of oocyte meiosis?

A

the LH surge at mid-point of menstrual cycle triggers oocyte maturation and the resumption of meiosis

184
Q

What are the process in Oocyte maturation?

A

corona radiate cells of the follicle retract their filopodia to break contact with the primary oocyte, cAMP level in the oocyte decreases, which activates the cyclin-dependent protein kinase MPF (maturation promoting factor)

185
Q

What is the completion of meiosis 1 marked by?

A

the formation of a secondary oocyte and the release of a polar body

186
Q

What are the different stages of the cell cycle in mitosis?

A

M
G1
S
G2

187
Q

What are the different cell stages in meiosis?

A
  • there is no S, G1 or G2

- and there is only one cyclin/ cyclin dependent kinase complex (MPF)

188
Q

What causes the arrest in diplotene?

A

an inactive or latent MPF (phosphorylated)
- the gap junction communication between corona radiate cells and the primary oocyte blocks activity of the MPF cyclin-dependent protein kinase

189
Q

How does LH pull out of diplotene?

A

pituitary LH causes the corona radiate cells to retract their filopodia and this decreases the cAMP and PKA activity in the oocyte to allow MPF activation and resumption of meiosis 1

190
Q

What occurs as oocytes complete meiosis 1?

A

nuclear membrane dissolves
chromosomes condense and move to the animal pole
asymmetric cell division results in large secondary oocyte and a small polar body

191
Q

How does the LH surfge affect the follicle?

A

stimulates secretion of proteases (collagenase and plasminogen activator) from the ovarian tissue surrounding the follicle and contraction of the surrounding smooth muscles
- this causes the mature follicle to rupture and release the secondary oocyte form the ovary

192
Q

What accompanies a secondary oocyte?

A

cluster of follicle cells called the cumulus layer

193
Q

Cytostatic factor

A

appears in the oocyte cytoplasm (maintains MPF in an active state by blocking degradation of its cyclin subunit) causing the secondary oocyte to arrest at meiosis in metaphase 2

194
Q

How does the oocyte progress past meiosis metaphase 2?

A

upon fertilization cytostatic factor is degraded triggered by an increase in Ca in the egg after fertilization

195
Q

What is the pathway for cytostatic factor degradation?

A

fertilization causes a calcium influx which increases calmodulin to trigger Cam-PKII and Calpain II both of which are proteases to degrade CSF

196
Q

Meroistic

A

a reference to tiny parts that are repeating

ACB- Development (2 decks)

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