gene expression Flashcards

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1
Q

universal

A

same 3 bases on triplet/codon code for the same amino acids in all organisms

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2
Q

non overlapping

A

each base is read as part of only one triplet/codon

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3
Q

degenerate

A

more than one triplet codes for an amino acid

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4
Q

mutations

A
  • substitution (silent)
  • addition (frame shift
  • chromosomal nondisjunction (chromosomes fail to split during metaphase 1. down syndrome caused by chromosome 21, 3 instead of 2 chromosomes)
  • inversion
  • duplication
  • translocation (bw non homologous chromosomes)
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5
Q

mutagenic agents

A

high energy ionising radiation (gamma rays, beta particles) interferes with dna replication
- dna reactive chemicals: benzene, hydrogen peroxide
- biological agents: viruses/ bacteria

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6
Q

totipotent stem cells

A

can give rise to complete human/all cell types
- translate only part of their DNA, producing specific proteins leading to cell specialisation
- divide by mitosis
- occurs during zygote, up to 8 cell stage

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7
Q

pluripotent

A
  • divide by mitosis
  • only translate part of their DNA
  • can only give rise to some cell types (ie: cells that make up tissue in the mammalian feotus)
  • embryonic and fetal stem cells
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8
Q

multipotent

A
  • exist in tissues
  • retain the ability to differentiate into a limited number of cell types (eg: bone marrow only RBCs and WBCs)
  • used for vital growth and repair of damaged tissues
  • adult stem cells
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9
Q

unipotent

A

give rise to only one type of cell
(eg: heart stem cells differentiate into cardiomyocytes)
- used for vital growth and repair of damaged tissues

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10
Q

key points

A
  • only stem cells can divide by mitosis
  • differentiation of stem cells determined by gene expression (only some parts of dna expressed, others inactive)
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11
Q

explain how cells produced from stem cells ahve the same genes yet be of different types?

A

not all genes are switched on/active
- gene expression involves transcription factors (proteins that bind a genes promoter region and either promote or inhibit the transcription of a gene)

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12
Q

describe the mechanism by which a signal protein causes the synthesis of mRNA

A
  • signal protein binds to the receptor on surface membrane
  • messenger molecule moves from cytoplasm and enters nucleas
  • activate transcription factor
  • binds to promoter region
  • RNA polymerase transcribes target gene
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13
Q

applications for stem cells

A
  • produces tissues for skin grafts
  • organ transplant research
  • research into how cells become specialised
  • cancer research
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14
Q

stem cell concerns

A
  • may divide rapidly out of control, forming tumours
  • embryos have human status from mone tof conception
  • not true human being, ebnefits outweigh risks
  • no moral rights
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15
Q

iPSC

A

induced pluripotent stem cells
- lab grown pluripotent cells prpduced from somatic cells using transcription factors
-capable of self renewal and limitless supply

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16
Q

promoter region

A

one or more base sequences found upstream of a gene
control the expression of that gene

17
Q

transcription factors

A

proteins, when activated, bind to the promoter region of the gene
stimulates RNA polymerase to begin transcription of the target gene

18
Q

describe how oestrogen enables RNA polymerase to begin transcription of its target gene

A
  • oestrogen diffuses via phospolipid cell membrane and diffuses through the nuclear envelope (is lipid soluble)
  • binds to the oestrogen receptor
  • changes the 3 structure of the receptor
  • releases transcription factor which binds to the dna
  • at the promoter region
  • stimulates RNA polymerase to transcribe the gene
19
Q

rna interference

A

miRNA = microRNA
small interfering RNA = siRNA
- single strand of miRNA and siRNA binds to a protein in cytoplasm to form a RISC (RNA-induced silencing) complex
- complementary base sequence to specific mRNA molecule

20
Q

RISC

A

RISC inhibits gene expression by binding to complementary mRNA; mRNA hydrolysed by enzyme into fragments OR initiation of ribosomal translation inhibited.
- translation doesnt take place, polype[tide not produced
- expression of gene silenced

21
Q

why might a protein still be present even after the introduction of RNAi?

A

not all mRNA has been destroyed
so some translation still occurs

22
Q

epigenetics

A

inheritable changes in gene expression
without changes in DNA base sequence
inhibits translation via methylation of DNA / acylation of histones

23
Q

compare the structure of dsRNA and DNA

A

dsRNA = double stranded RNA
- polymer of nuclepotides
- A,C and G
pentose sugar
double stranded
- dsRNA contains U, DNA contains T
- dsRNA ribose DNA deoxyribose
dsRNA shorter than DNA

24
Q

explain how methylation of tumour suppressor genes can lead to cancer

A

-methylation prevents transcription of a gene
-protein that prevents cell division not produced
-no control of mitosis

25
Q

process of methylation

A

CH3 added to c5 of cytosine base
methyltransferase enzyme catalyses this reaction
cpg islands silence genes by preventing TF binding to promoter

26
Q

process of acetylation of histones

A

DNA in chromosomes wrapped around histones creating nuclosomes
- become loosely packed so dna less condensed
- promoter regions are exposed TF bind
- RNA polynerase to bind an dtranscribe target gene

27
Q

describe how alterations of tumour suppressor gene can lead to development of tumours

A
  • increased methylation of TSG
  • mutation in TSG
  • TSG not transcribed
  • uncontrolled cell division
28
Q

DESCRIBE what is meant by a MALIGNANT tumour

A

mass of undifferentiated cells
- uncontroled cell division
- metastasis forms new tumours
- spread to other parts of body
- fast growing
- non capsulated

29
Q

describe benign tumours

A

surrounded by a capsuke
dont metastasise
slow growing

30
Q

describe how altered DNA can lead to cancer

A
  • dna altered by mutation
  • mutation changes base sequence
  • of gene controlling cell growth (oncogene)
    -of TSG
    changes protein structure
    TSG produces proteins that inhibit cell division
  • mitosis: uncontrolled cell division forming malignant tumours
31
Q

define epigenetics

A

heritable changes not involving changes in DNA base sequence

32
Q

proto-oncogenes

A

stimulate cell division
codes for proteins that increase rate of CD

33
Q

Tumour suppresor genes

A

slow cell division
code for proteins decreasing rate of CD
- code for proteins repair mistakes in DNA
- code for proteins instructing cells to die
eg: BRCA2, TP53

34
Q

mutations in genes

A

proto oncogene mutation causes oncogene
- overstimulation of cd so persmanently switched on

tsg mutation = inactivated
- stops inhibiting cd, rate of cd increases

35
Q

epigenetic changes to TSG

A

increased methylation of tsg increases rate of cd
increased acetylation of tsg decreases rate of cd

36
Q

epigenetic changes to oncogene

A

decreased methylation increases rate of cd
decreased acetylation of histones decreases rate of cd