Gene Expression Flashcards

(23 cards)

1
Q

What are totipotent cells, and what can they do?

A

Totipotent cells can differentiate into any cell type, including extraembryonic tissues.

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2
Q

How do totipotent cells contribute to cell specialisation?

A

Totipotent cells express only certain genes, leading to specialisation.

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3
Q

How long do totipotent cells remain in a mammalian embryo?

A

Totipotent cells exist only in early embryonic stages before differentiating into other stem cells.

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4
Q

Where are pluripotent, multipotent, and unipotent cells found?

A

Pluripotent cells (embryos) form any body cell, multipotent cells (adults) form a limited range, and unipotent cells form one type.

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5
Q

How can pluripotent stem cells be used in treating human disorders?

A

Pluripotent stem cells can be used to treat disorders by replacing damaged tissues (e.g., nerve cells for Parkinson’s).

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6
Q

What are unipotent cells, and how do they relate to cardiomyocytes?

A

Unipotent cells form one cell type, e.g., cardiomyocytes, which help regenerate heart tissue.

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7
Q

How are induced pluripotent stem cells (iPS cells) created?

A

iPS cells are created by reprogramming adult somatic cells using transcription factors.

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8
Q

What are the ethical and medical considerations in using stem cells for treatment?

A

Stem cell treatments raise ethical concerns (embryo use) but have medical potential (regenerative medicine).

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9
Q

How can transcription be stimulated or inhibited in eukaryotic cells?

A

Transcription factors move into the nucleus to stimulate or inhibit transcription.

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10
Q

What is the role of oestrogen in initiating transcription?

A

Oestrogen binds to transcription factors, enabling them to activate specific genes.

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11
Q

What is epigenetics, and how does it regulate gene expression?

A

Epigenetics involves gene expression changes without altering the DNA base
sequence.

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12
Q

How does DNA methylation affect transcription?

A

Increased DNA methylation prevents transcription by blocking RNA polymerase binding.

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13
Q

How does histone acetylation affect transcription?

A

Decreased histone acetylation causes tighter DNA packing, inhibiting transcription.

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14
Q

How does epigenetics contribute to disease development and treatment, particularly in cancer?

A

Epigenetic changes can silence tumour suppressor genes or activate oncogenes, leading to cancer.

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15
Q

What is RNA interference (RNAi), and how does it affect gene expression?

A

RNAi prevents translation by degrading or blocking mRNA.

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16
Q

What are the key characteristics of benign and malignant tumours?

A

Benign tumours grow slowly, remain localised, and don’t invade tissues, while malignant tumours grow rapidly and spread (metastasis).

17
Q

What is the role of tumour suppressor genes and oncogenes in cancer?

A

Tumour suppressor genes slow cell division, while oncogenes promote cell division. Mutations cause uncontrolled growth.

18
Q

How does abnormal methylation of tumour suppressor genes and oncogenes contribute to cancer?

A

Hypermethylation of tumour suppressor genes silences them, while hypomethylation of oncogenes activates them, leading to cancer.

19
Q

How does increased oestrogen concentration contribute to breast cancer development?

A

Increased oestrogen stimulates excessive cell division in breast tissue, increasing cancer risk.

20
Q

How can an understanding of oncogenes and tumour suppressor genes be used in cancer prevention, treatment, and cure?

A

Understanding oncogenes and tumour suppressor genes helps develop targeted therapies for cancer treatment.

21
Q

How can data be used to interpret gene expression investigations?

A

Gene expression data can be analysed by comparing RNA levels, protein levels, or gene mutations.

22
Q

How can we evaluate genetic vs environmental influences on phenotype?

A

Genetic vs environmental influences can be determined through twin studies, population data, and mutation analysis.

23
Q

How can evidence be used to evaluate correlations between genetic and
environmental factors in cancer?

A

Cancer correlations can be evaluated by analysing genetic mutations, environmental exposures, and epidemiological data.