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B8. Gene Expression > Gene Expression > Flashcards

Gene Expression Flashcards

1
Q

What are mutations?

A

Changes to the nucleotide sequence of DNA during DNA replication (interphase)

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2
Q

Ways mutagenic agents increase rate of mutations

A
  • Base analogs / acting as a base (chemicals substitute for a normal nucleotide base)
  • Altering bases (chemicals delete/alter base)
  • Changing DNA structure (chemicals/radiation change DNA structure)
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3
Q

Types of mutations

A
  • Substitution (swapping one base for another)
  • Addition (extra base added)
  • Deletion (base is removed)
  • Inversion (sequence of bases is reversed)
  • Duplication (one or more bases are repeated)
  • Translocation (sequence of bases is moved from one part of the genome to another)
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4
Q

How may a mutation cause a change to a single AA?

A
  • Changes one DNA triplet
  • Changes the translation of one amino acid
  • Changes the primary structure of the protein
  • Changes the hydrogen / ionic bonding
  • Changes the tertiary structure of the protein
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5
Q

How may a mutation cause a change to many AA?

A
  • Frame shift changes the sequence of all following DNA triplets
  • Changes the translation of all following amino acid
  • Changes the primary structure of the protein
  • Changes the hydrogen / ionic bonding
  • Changes the tertiary structure of the protein
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6
Q

Which genes control cell division?

A

Tumour suppressor genes and proto-oncogenes. Mutations to these genes can cause cancer

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7
Q

Tumour suppressor genes

A
  • Make proteins that slow down rate of mitosis or speed up rate of apoptosis
  • Mutation to a tumour suppressor gene may lead to a non-functional protein
  • Non-functional protein means cells divide uncontrollably
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8
Q

Proto-oncogenes

A
  • Make proteins that increase rate of mitosis
  • If proto-oncogene mutates it becomes an oncogene
  • Oncogenes can be over expressed resulting in uncontrollable cell division
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9
Q

Types of tumours

A
  • Benign (non-cancerous, grow slowly, harmless)
  • Malignant (cancerous, grow quickly, destroy tissues, spread in blood)
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10
Q

Identifying tumour cells

A
  • Larger, darker nucleus (sometimes multiple)
  • Irregular shape
  • Different antigens on surface
  • Divide (mitosis) more frequently
  • Don’t produce all proteins needed to function correctly
  • Don’t respond to growth regulating processes
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11
Q

Role of abnormal methylation in tumour growth

A
  • Hypermethylation of tumour suppressor genes means proteins that slow cells division are not transcribed, resulting in uncontrollable cell division
  • Hypomethylation of proto-oncogenes causes them to act as oncogenes, so more proteins that speed up cell division are transcribed, resulting in uncontrollable cell division
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12
Q

Role of oestrogen in breast cancer

A
  • Oestrogen-oestrogen receptor complex can activate transcription of oncogene
  • Oestrogen can increase rate of cell division and thus DNA replication so mutations more likely
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13
Q

What are stem cells?

A

Unspecialised cells that can divide and differentiate into different types of specialised cells

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14
Q

Types of stem cells

A
  • Totipotent (differentiate into ANY type of specialised cell, found in early mammalian embryos)
  • Pluripotent (differentiate into MANY type of specialised cell, found in mammalian embryos)
  • Multipotent (differentiate into FEW type of specialised cell, found in adult bone marrow)
  • Unipotent differentiate into ONE type of specialised cell, found in adult bone marrow)
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15
Q

How do stem cells become specialised?

A

Conditions within cells control which genes are expressed (transcribed + translated into proteins)

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16
Q

Obtaining induced pluripotent stem cells (iPS cells)

A
  • Use a modified virus as a vector
  • Virus inserts transcription factor genes from pluripotent cells into the DNA of unipotent stem cells
  • Transcription factors are expressed, making the unipotent stem cells pluripotent
17
Q

Obtaining embryonic stem cells

A
  • Embryos made in a lab by IVF
  • Pluripotent stem cells are removed after a few days
  • Embryo is destroyed
  • Pluripotent stem cells can differentiate into most types of body cells (not placental cells)
18
Q

Obtaining adult stem cells

A
  • Removed from the bone marrow of adults in operation
  • Multipotent stem cells can differentiate into some types of body cells
19
Q

How are stem cells used in medicine?

A
  • Bone marrow transplants (multipotent stem cells can differentiate into healthy blood cells)
  • Growing new organs (iPS cells, genetically identical, avoiding rejection)
20
Q

Ethical issues of stem cells

A
  • Taken from IVF embryos which could develop into a foetus if implanted
  • From fertilisation zygote has right to live
  • Adult stem cells are not totipotent or pluripotent
21
Q

What are transcription factors?

A

Proteins that control rate of protein synthesis by switching some genes on/off. These can be activators or repressors

22
Q

How do transcription factors work?

A
  • Transcription factors move from the cytoplasm into the nucleus
  • Binds to the promoter region of DNA at the start of the gene
  • Activators help RNA polymerase bind to DNA so the gene is transcribed
  • Repressors prevent RNA polymerase binding to DNA so the gene is not transcribed
23
Q

Role of oestrogen in controlling transcription factors

A
  • Oestrogen (steroid hormone) enters cytoplasm through phospholipid bilayer as lipid soluble
  • Oestrogen binds to a TF called an oestrogen receptor, forming an oestrogen-oestrogen receptor complex
  • Complex binds to promoter region of DNA, initiating transcription
24
Q

What is RNA interference (RNAi)?

A

Small double stranded RNA molecules stop mRNA from target genes being translated into proteins

25
Q

siRNA

A
  • siRNA combines with proteins to form a siRNA-protein complex
  • siRNA unwinds becoming single stranded
  • siRNA binds to mRNA by complimentary base pairing
  • siRNA-protein complex breaks down the mRNA into pieces, preventing translation
  • mRNA pieces are recycled
26
Q

microRNA

A
  • microRNA combines with proteins to form a microRNA-protein complex
  • microRNA binds to mRNA by complimentary base pairing
  • miRNA-protein complex prevents ribosome attaching, preventing translation
27
Q

What is epigenetics?

A

Heritable changes in gene expression without changing the base sequence of DNA caused by changes in the environment that inhibit transcription

28
Q

Methylation of DNA

A
  • Methyl (-CH3) can attach to DNA at CpG sites in DNA
  • Methylated CpG sites prevent transcription enzymes attaching, preventing transcription
  • More methylation terminates transcription
29
Q

Acetylation of histones

A
  • Acetyl groups make histones space out (DNA is less tightly coiled)
  • Allows transcriptional enzymes to attach so gene can be expressed
  • Enzymes remove acetyl groups, preventing transcription
  • Less acetylation of histones terminates transcription

B8. Gene Expression (2 decks)

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