Topic 8 Flashcards

(18 cards)

1
Q

Stem cells

A

.Undifferentiated cells which can continually divide and become specialised cells

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2
Q

Different types of stem cells (4)

A

Totipotent - Can differentiate into any type of body cell, occur in early stages of mammalian embryos, only translate 1 part of DNA to become specialised
Pluripotent - Can differentiate into most cells (not placenta cells) - in embryo
Multi-potent - Can differentiate to form a limited number of cells - found in bone marrow
Unipotent - Only differentiate to form one type of cell

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3
Q

Problem with using stem cells

A

.As they continually divide, they can form tumours
.Therapeutic cloning (unlike reproductive cloning, we don’t clone to make a living individual, we clone to make stem cells)
.Destroying the embryo (debate on of it is destroying a life)

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4
Q

What are IPS

A

Induced pluripotent cells, made from using transcription factors to switch on genes on unipotent cells , making pluripotent stem cells

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5
Q

Epigenetics and what causes it

A

.Heritable changes in gene function without changing DNA base sequence
.Factors such as diet, stress and toxins can add chemical tags to DNA/Histones (CHANGES THEIR EPIGENOME)

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6
Q

Difference between heterochromatin and chromatin

A

Heterochromotin is tightly coiled (gene will not be transcribed) whereas chromotin is loosely coiled ( Gene will be transcribed)

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7
Q

What are transcription factors

A

These are protein found in the cytoplasm which move into the nucleus and bind to a complimentary base sequence (promotor region) to turn on/turn off genes (it allows RNA polymerase to bind DNA )
Without binding of transcription factors, the gene is INACTIVE (turned off)

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8
Q

Describe Methylation

A

When methyl groups attach to cytosine base on DNA, Increased methylation results in heterochromatin (due to positive charge) so inhibits transcription by preventing transcriptional factors from binding

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9
Q

Describe acetylation

A

Bind to the histones, and due to negative charge they repel DNA (causing it to be loosely packed) allowing for transcription factors to bind.

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10
Q

What are tumour suppressor genes and what are oncogenes

A

.Genes which produce proteins that slow down (regulate) cell division and cause cell death if copying errors are detected
.Oncogenes creates a protein which triggers mitosis to occur.

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11
Q

Why is breast cancer more likely after menopause

A

Fat cells in breast tissue start to produce oestrogen, which can bind to transcription factor which turns on a proto-oncogene, if this is permanently switched in cell division occurs uncontrollably.

.This is an example of positive feedback as more breast tissue is made and this increases concentration of oestrogen even more.

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12
Q

Whats the role of Oestrogen

A

This is a steroid hormone (meaning it’s lipid soluble and can simply diffuse from the blood into the cell) which binds to the receptor site on the transcriptional factor , cause DNA binding site to change shape slightly, making it complementary to DNA and able to bind

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13
Q

What is the role of RNAi

A

The prevent translation by destroying mRNA

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14
Q

How is siRNA (small interfering RNA) made

A

dsRNA (double stranded RNA) is cut into small sections by an enzyme, making siRNA

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15
Q

How does siRNA prevent translation

A

One strand of siRNA combines with an enzyme to form an siRNA-enzyme complex which will bind to complementary base sequence in mRNA , and the mRNA is cut up so it CAN NOT BE TRANSLATED)

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16
Q

differences between Benign tumour and malignant tumours (5)

A

. Benign tumour grow at a slow rate whereas malignant grow rapidly ( due to them being able to grow projections into the blood supply as they have no capsule and so they obtain oxygen and glucose)

. Benign tumour produce adhesive molecules, sticking them together to a particular tissue whereas malignant don’t produce adhesive molecules so break off and spread to other parts of the body

. Benign tumour are surrounded by a capsule so they remain compact whereas malignant are contained in a capsule

. Benign tumour can be removed from surgery and rarely return whereas malignant recurrence is much more likely

. Benign tumours impact is localised whereas malignant effect is systematic

17
Q

How tumours can develop

A

.Increased oestrogen concentration
.Gene mutation in tumour suppressor gene
.Gene mutation on oncogene
.Abnormal methylation of tumour suppressor genes (increased methylation) or oncogene (decreased methylation)

18
Q

What are proto-oncogene gene and oncogenes

A

.Oncogenes are mutated proto-oncogenes (cells divide continually as its permanently activated)
.Proto-oncogenes is a protein which initiates DNA replication