The developing Cell Flashcards by Francisco Campino

Cell cycle

Cell growth, maturity and division
This is the process that all somatic cells in multicellular organisms use to grow and divide

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Cell cycle 3 stages

interphase, mitosis, cytokenesis

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Interphase

not part of mitosis

Growth 1- Cells grow in size & mass, organelles replicated, inc protein synthesis *(chloroplasts & mitochondria not replicated)

Synthesis- DNA replication using SCR

Growth 2- energy stores increase, cell continues to increase in size & mass, chloroplasts & mitochondria increase in size and divide

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What does G1 checkpoint check for

-Chemicals needed for replication present
-Damage in DNA before synthesis
-Suitable in size
-Sufficient nutrients

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What does G2 checkpoint check for

-All DNA has replicated without damage
-Cell is of correct size

Otherwise, daughter cells will not receive identical genetic information

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Mitosis

Nuclear division- produces 2 genetically identical nuclei

Are them distributed unto two genetically identical daughter cells

I push miss around the corner

prophase, metaphase, anaphase, telophase

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Prophase

(preparing)

-Chromosome condense (can now be seen easier)
-Each chromosome consists of 2 sister chromatids joined by a centromere
-Centrioles move towards poles
-Spindle fibres form
-Nucleolus & nuclear envelope breaks down

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Metaphase

(middle)

-Chromosomes line up against the equator
-Spindle fibres attach to centromere

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Anaphase

(pulled Apart. Arrow heads)

-Spindle fibres contract
-Centromere splits
-Daughter chromosomes pulled to opposite poles, centromere first

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Telophase
(Two)

-Daughter chromosomes reach poles
-Chromosomes uncoil & lengthen
-Spindle fibres disintegrate
-Nuclear envelope & nucleolus reforms

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Summary of mitosis

Animal Plant
most tissue. meristematic only
cell becomes round no change
Centrioles No
Spindles disappear Remain
Microfilaments No

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Some cells lose ability to divide

eg. neurones, muscle cells

They leave the cycle temporarily or permanently due to:

a) Differentiation
b)Damaged DNA. Cell no longer viable so enter G0.

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Importance of mitosis

-Growth of multicellular organisms
-repir damaged tissues
-replacement of cells
-asexual reproduction

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Homologous chromosomes

46 (23 pairs)
Each pair is made up of one maternal and one paternal

Same: sequence of genes, same length, position of centromere
Different: Origins, alleles

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how do we analyse the cell cycle?

flow cytometry:
- DNA stained with fluorescent dye
- passed through flow cytometer
- fluorescent intensity recorded

more DNA = more fluorescence ∴ increases G1 -> S -> G2

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Cells which do not carry out mitosis

Mature RBC, neurones

Cell cycle control

Sequence & timing controlled by cyclins (protein)

which activate enzymes called cyclin-dependent kinases

which catalyse the addition of a phosphate group onto a protein, changing its tertiary structure

Specific CDKS control specific steps in cel cycle

What happens if errors are detected during cell cycle

p21 binds to CDKs
idea of complementary, blocks active site
This halts cell cycle at G1 stage in interphase

without p21, cancer. It is a tumour suppressor gene

Mutations to cyclin genes or CDKs can lead to failure to repair DNA-> cancer

Cytokenesis

Process of cytoplasm and two nuclei being divided to physically form 2 new daughter cells

Cytokenesis in animal cells

-CSM invaginates
-Cleaveage furrow forms in middle of cell
-csm pinches until 2 sides meet
-Cytoplasm & organelles are divided equally into 2 new daughter cells

Cytokenesis in plant cells

-Only in meristematic tissue
-vesicles from Golgi assemble on the equator= cell plate
-vesicles fuse with one another and the csm
-Cell wall forms along middle lamella
-Cytoplasm & organelles are divided equally into 2 new daughter cells
-Plant cells are inelastic due to cellulose cell wall

Synoptic link with cell cycle and cancer

-Negative regulator molecules (p53, p21) act primarily in G1 checkpoint and prevent cell from moving forward to synthesis until DNA is repaired

-p53 halts the cell cycle and recruits enzymes to repair DNA. If it cannot be repaired, apoptosis is initiated

Apoptosis

-Programmed cell death
(ordered and controlled process)

Necrosis

-unregulated cell death after trauma
-surface membrane ruptures, release of hydrolytic enzymes

Control of apoptosis

Cell signals are received from inside & outside of cells -signals: p53, cytokines, hormones, growth factors etc -Different signals induce apoptosis in different tissues

Apoptosis

-cell shrinks & chromatin in nucleus condenses (pyknosis) -CSM breaks down & blebs form -DNA breaks down -Cell organelles break down -Cell fragments into apoptotic bodies -Macrophages engulf cell fragments

Uses of apoptosis

-fetal eg. toes -puberty -immune system (destruction of harmful immune cells) -Formation of connections between neurones in brain

Stimuli

internal: eg. DNA change. Damage detected by cyclins, hals cell cycle -> apoptosis external: attack by a pathogen

Detecting apoptosis & necrosis

-Flow cytometry -Annexin V is used to detect apoptotic cells -Binds to phosphatidylserine, a marker of apoptosis when in monolayer nectrotic late apoptotic Live ealy apoptotic

Stem cells

Unspecialised Are potent Can differentiate into specialised cells

Cell specialisation

At day 19, cells differentiate, producing specialised cells Genes are switched on/off Cells divide by mitosis to produce genetically identical clones Groups of cells form tissues Groups of tissues form Organs

Properties of stem cells

self-renewal: ability to divide many times while maintaining an unspecialised state potency: ability to differentiate into specialised cells

Totipotent cells (The prime minister)

Can form all cells in the body plus placental cells Source: very early embryos, meristematic tissue

Pluripotent cells

Can form all cells in body but not placental cells source: inner cell mass of blastocyst eg use: cell replacement therapies- produce pancreatic cells to treat diabetes

Mutipotent cells

Adult stem cells can give rise to a limited number of cell types. source: bone marrow, bone, umbilical chord eg. uses: treat leukaemia, blood cancers, bone cancers

Problems with stem cells therapies

-Embryo rights, destruction of human embryos, hasn't produced any viable long term treatments -Better to turn differentiated cells back into pluripotent

Process of stem cell differentiation

-stem Cells undergoes mitosis -Genes are switched on/off -New proteins made -cell becomes specialised