BIOLOGY 1A Lecture Notes - Lecture 28: Adult Stem Cell, Stem Cell, Unipotent

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11 Jun 2018

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DEVELOPMENT 1: STEM CELLS AND CELL FATE

Development= events in changing from simple to more complex form

4 sub-processes:

Cell division

Differentiation

Pattern formation

Morphogenesis: shape of body changes

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Cell differentiation

Genomic equivalence= all cells in the body have same genetic material

Humans have 210 major cell types

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Differentiation= cell becomes more specialized in structure and function

Ex: Muscle and nerve cells have different structure and function

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Cell determination= potential fates become more limited until cell is

'committed' to its fate

Potential of a cell to become different types of cells

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Molecular basis of determination

Differential inheritance of cytoplasmic determinants

Cell-cell communication

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•

Stem cells give rise to differentiated cells

Stem cells are capable of continued division, and can give rise to

differentiated cells

Degrees of determination differ:

Totipotent: give rise to any tissue in an organism

Embryo and extra-embryonic

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Pluripotent: give rise to all cells in the adult

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Multipotent: give rise to limited number of cells

Not all cell types ex. bone marrow

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Unipotent: give rise to only a single cell type

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Embryonic stem cells are pluripotent whereas adult stem cells are multipotent

Put needle in embryo in inner cell mass and take cells out for culture

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The discovery of growth factors that control cell determination and growth

Levi-Montalcini and Cohen

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Took tumor cells from a mouse and put it into chick embryo. Huge over

proliferation of neurons in chick. What is produced by tumor cells for

overproduction of neurons?

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Discovery of Nerve Growth Factor (NGF) (peptide growth factor)

Sensory ganglion dissected from chick embryo---> secreted proteins from

tumor cells added to chick embryo----> nerve outgrowth!

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The nematode Caenorhabditis elegans is a model organism for studying

development

Model organism= organism selected for study as representative of a large

group of species

One of the most completely described models of development

Adult worm consists of 959 somatic cells

Transparent, so division can be followed

Lineage of cells mapped

Fate of each cell is same in every individual

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•

Identifying genes involved in vulva cell fate determination

Isolated mutants missing vulva--> map and sequence mutated gene-->

identified growth factor and receptor

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Epidermal growth factor (EGF) and its receptor (EGFR) in vulva cell fate

Anchor cell secretes inducer that influences vulva cell fate

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PARACRINE SIGNALING

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Cells closer to anchor cell receives higher concentration of EGF

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Anchor cell secretes EGF--> Activates EGF receptor--> High EGF promotes

primary fate---> Lower EGF promotes secondary fate

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Depending on how much of growth factor received--> different fates for

the cell

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THEME 2 IN SIGNAL TRANSDUCTION: PROTEIN PHOSPHORYLATION

On/off switch•

Protein kinases: phosphorylate groups to turn it on •

Protein phosphatases: remove phosphate groups to turn it off•

On/off state can either be phosphorylated or not•

Epidermal growth factor receptor is a receptor tyrosine kinase (RTK)

Inactive1.

Ligand binding (EGF secreted by anchor cell) --> dimerization

Two receptor's phosphorylates the other on tyrosinei.

Phosphorylation on tyrosine3.

Protein binding --> signal transduction

Bind to tyrosine residue that causes a responsei.

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Cell fate determination is reversible

John Gurdon, Shinya Yamannaka (iPS cells)

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Nuclear reprogramming= nucleus from differentiated cell undergoes

changes to de-differentiate and allow it to direct development

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Similar to John Gurdon:•

Somatic cell nuclear transfer in mammals

Mammary cell donor donates mammary cells which are cultured1.

Egg cell donor donates egg cell from ovary from which the nucleus is

removed

Fuse mammary cell with egg cell donor to create nucleus from mammary

cell

Nucleus is de-differentiatedi.

Nucleus from mammary cell is grown in culture to create early embryo4.

Early embryo is implanted in uterus of 3rd sheep (surrogate mother)5.

Embryonic development occurs and Lamb "Dolly" is genetically identical

to mammary cell donor

Shinya Yamannaka•

Reprogramming adult cells into iPS cells

Stem cell--> precursor cell ------> Skin fibroblast cell

Add 4 stem cell master regulator genes, Oct 3/4, Sox2, Klf4, cy-Myc

INDUCES PLURIPOTENT (iPS) CELL

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Lecture 28-4/4

Monday, April 9, 2018

4:54 PM

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Document Summary

Development= events in changing from simple to more complex form. Genomic equivalence= all cells in the body have same genetic material. Differentiation= cell becomes more specialized in structure and function. Ex: muscle and nerve cells have different structure and function. Cell determination= potential fates become more limited until cell is. Potential of a cell to become different types of cells. Stem cells are capable of continued division, and can give rise to differentiated cells. Totipotent: give rise to any tissue in an organism. Pluripotent: give rise to all cells in the adult. Multipotent: give rise to limited number of cells. Unipotent: give rise to only a single cell type. Embryonic stem cells are pluripotent whereas adult stem cells are multipotent. Put needle in embryo in inner cell mass and take cells out for culture. The discovery of growth factors that control cell determination and growth. Took tumor cells from a mouse and put it into chick embryo.

Related Questions

Which of the following statements about stem cells are true.

CHECK ALL THAT APPLY

When a stem cell divides, each new cell has the potential either to remain a stem cell or become another type of cell with a more specialized function.

Stem cells are unspecialized cells capable of renewing themselves through cell division, sometimes after long periods of inactivity.

Stem cells, under certain physiologic or experimental conditions, can be induced to become tissue- or organ-specific cells with special functions.

Stem cells have the remarkable potential to develop into only one single cell type in the body during early life and growth.

Summary

please!

Multipotent versus restricted

Morphologically detectable neural crest cells usually are first observed as the cells individualize and delaminate upon emigration from the neural tube, following their epithelial to mesenchymal transition (EMT), in which they convert from a tightly adherent sheet of cells to a dispersed and more individual mesenchymal population. Prior to EMT, however, it is difficult or impossible at most axial levels and in most species to distinguish presumptive neural crest cells from cells that will form dorsal neural tube derivatives. However, there are exceptions, such as a subpopulation of cranial neural crest cells in chick and mouse that appears to be set aside and morphologically distinct at midbrain levels. In addition, some species such as axolotl have a clearly segregated population of neural crest cells that exists as a ridge on the dorsal neural tube.

A long-standing debate in the neural crest literature has been whether neural crest cells are multipotent and/or restricted in their developmental potential. In other words, can a single neural crest precursor form only one type of derivative or are the cells multipotent and able to produce multiple derivatives. Single cell lineage experiments (Bronner-Fraser and Fraser, 1988), in which individual cells within the chick dorsal neural tube are labeled with vital dye, show that some of the labeled clones contribute to multiple differentiated cell types in the periphery, including melanocytes, sympathetic and sensory ganglion cells. Thus, the original precursor was âmultipotentâ in its developmental potential to form neural crest derivatives. In addition to neural crest derivatives, single dorsal neuroepithelial cell also give rise both to migrating neural crest cells and cells that remain in the dorsal neural tube, such as roof plate cells and dorsal sensory neurons and/or interneurons. This suggests a shared lineage between the neural tube and neural crest, at least at this stage. However, labeling migrating neural crest cells in vivo also produced clones that could contribute to more than one neural crest lineage (Fraser and Bronner-Fraser, 1991), again supporting the idea that some of the migrating population retained multipotency.

Clonogenic culture of neural crest cells cultured shortly after their emigration from the neural tube definitely shows that many early migrating neural crest cells are multipotent in vitro as well (Baroffio et al., 1988, Calloni et al., 2007, Calloni et al., 2009, LeDouarin et al., 2008a, LeDouarin et al., 2008b, Sieber-Blum and Cohen, 1980 and Stemple and Anderson, 1993). Exposure to different growth factors can profoundly influence their lineage decisions (e.g. Lahav et al., 1998). Furthermore, they have a capacity for self-renewal, at least for a few cell divisions (Stemple and Anderson, 1993 and Trentin et al., 2004).

The fact that individual neural crest cells can form multiple derivatives has led to the idea that they have stem cell properties. Stem cells are defined as individual progenitor cells that can generate one or more specialized cell types. A cardinal feature of stem cells is their ability to self-renew, that is, to divide so as to give rise to at least one daughter cell that maintains the multipotent character of its parent. The fact that cloned neural crest cells have a limited ability to self-renew has led to the idea that they are stem-like (progenitors) cells rather than true stem cells. Interestingly, however, neural crest stem cells can be derived from adult tissues (Fernandes et al., 2008 and Shakhova and Sommer, 2010; see Chapter Dupin and Sommer), suggesting that they can remain quiescent for long periods of time or maintain long term self-renewal ability when left in situ.

The presence of some multipotent neural crest precursors cannot, however, rule out the possibility that other precursors may be more restricted in their developmental potential. In fact, experiments in zebrafish suggested that neural crest cells contribute to different sets of derivatives accordingly to their migration order (Raible and Eisen, 1994). However, if the leader cell was ablated, the next cell in line took up the fate that would have been filled by the ablated cell (Raible and Eisen, 1996). Similarly, early migrating neural crest cells normally exhibit a broader range of derivatives than later migrating cells; however, when the early population is ablated and replaced by late migrating cells, the late migrating cells assume a broader developmental potential than that prescribed by their normal fate (Baker et al., 1997). This raises a very important issue: that developmental potential is greater than or equal to a cell's normal fate. Only by challenging the cell by putting it into a new environment can one test for restriction of cell fate. This is best exemplified by experiments in which the potential of neural crest populations was challenged by performing heterotopic transplants between different axial levels (LeDouarin and Teillet, 1974), such as exchanging cranial and trunk, or vagal and trunk populations. The results demonstrate a combination of flexibility in cell fate and some axial level-autonomous characteristics. For example, cranial neural crest cells normally make cartilage and bone of the face whereas trunk neural crest cells do not. Transplantation of cranial neural folds to the trunk results in production of many normal trunk derivatives, as well as the formation of ectopic cartilage nodules (Le Lievre et al., 1980 and LeDouarin and Teillet, 1974). Conversely, transplantation of trunk neural folds to the head results in contributions to cranial neurons and glia of cranial ganglia, but not to cartilage, although some connective tissues and pericytes derive from this graft (Nakamura and Ayer-le Lievre, 1982). This reveals some flexibility in fate, but a more limited ability to form skeletal derivatives (LeDouarin et al., 2004). However, trunk neural crest cells can form cartilage in vitro under appropriate culture conditions (Calloni et al., 2007 and McGonnell and Graham, 2002). Because challenging prospective neural crest fate is a difficult experiment, it is much easier to prove multipotency than restricted cell fate, leaving the question of whether or not there are lineage-restricted neural crest precursors still open to debate (see Krispin et al., 2010).

1. When does differentiation begin in fruit fly (insects)?

a. Prior to fertilization

b. Just after fertilization, but before any cell divisions takeplace

c. Just after the first cell division

d. At the blastula stage

e. At the globular embryo stage

2. When does differentiation begin in frog (vertebrates)?

a. Prior to fertilization

b. Just after fertilization, but before any cell divisions takeplace

c. Just after the first cell division

d. At the blastula stage

e. At the globular embryo stage

3. When does differentiation begin in flowering plants?

a. Prior to fertilization

b. Just after fertilization, but before any cell divisions takeplace

c. Just after the first cell division

d. At the blastula stage

e. At the globular embryo stage

4. Which axis develops first in animals, anterior-posterior(A-P) or dorsal-ventral (D-V)?

a. A-P

b. D-V

c. They develop at the same time.

d. They are controlled by the same transcription factors at thesame time.

5. Which axis develops first in plants, anterior-posterior ordorsal-ventral?

a. A-P

b. D-V

c. They develop at the same time.

d. Plants only develop A-P, and with respect to gravity andlight.

6. Focusing in on A-P development in Drosophila, maternaltranscription factors produce

proteins that control axis development in what order?

a. bicoid and nanos proteins; caudal and hunchback proteins; gapand pair-rule

proteins

b. caudal and hunchback proteins; bicoid and nanos proteins; gapand pair-rule

proteins

c. gap and pair-rule proteins; bicoid and nanos proteins; caudaland hunchback

proteins

d. gap and pair-rule proteins; caudal and hunchback proteins;bicoid and nanos

proteins

7. What ultimately controls pattern formation in Drosophila?

a. Morphogen gradients and signaling molecules under maternalcontrol

b. Morphogen gradients and signaling molecules under embryoniccontrol

c. De-repressors and signaling molecules under maternalcontrol

d. De-repressors and signaling molecules under embryoniccontrol

PLANT STRUCTURE, CELLS, CELL WALLS, PLASMODESMATA

8. Which of the following cannot be found in leaves?

a. Xylem

b. Phloem

c. Mesophyll

d. Parenchyma

e. Apical meristem

9. What are intercalary meristems?

a. Meristems that develop between internodes in some plants

b. Meristems that develop primary meristematic tissues

c. Meristems that are responsible for secondary growth in woodyplants

d. Root meristems

10. Roots, shoots, and leaves all contain three basic tissuesystems. What are they?

a. Ground, structural, conductive

b. Ground, vascular, dermal

c. Vascular, dermal, structural

d. Conductive, transmissive, supportive

11. All growth in plants is due to

a. Cell division in the three basic tissue systems andsubsequent cell elongation

b. Cell division at meristems and subsequent cell elongation

c. Cell division as needed throughout the plant body, followedby cell elongation

d. Hormone-induced cell division throughout the plant body

12. Which plant cells are dead at maturity, although stillproviding some useful function?

a. Dermal

b. Ground

c. Xylem

d. Phloem

e. Lateral meristems

13. Which meristems are responsible for lateral growth (increasein girth)?

a. Apical meristem

b. Root meristem

c. Vascular and bark cambium

d. Intercalary meristem

14. Where are most guard cells generally located in vascularplants?

a. Stem dermal tissue

b. Root dermal tissue

c. Petiole dermal tissue

d. Undersides of leaves

e. Uppersides of leaves

15. How can you distinguish guard cells from non-guardcells?

a. They contain mitochondria

b. They contain chloroplasts

c. They do not have plasmodesmata

d. They have plasmodesmata

e. B and C

PINs, IAA, ACID GROWTH

16. What are PINs?

a. Plasma membrane transport inhibitors

b. Auxin efflux transporters for active transport across plasmamembranes

c. Growth regulators

d. Hormones

e. Membrane transport proteins for embryogenesis

17. What is IAA?

a. Cytokinen

b. Gibberellic acid

c. Florigen

d. Auxin

e. Abscissic acid

18. Which hormone can trigger cell wall expansion?

a. Cytokinen

b. Gibberellic acid

c. Florigen

d. Auxin

e. Abscissic acid

19. Which ion is used by plants to decrease pH and activateenzymes that break cress-bridges

between cellulose fibers for cell wall expansion?

a. Na

b. K

c. Cl

d. H

e. Mg

20. Where do the ions come from to cause acidification of thecell wall?

a. Apoplast

b. Cytoplasm

c. Chloroplasts

d. Mitochondria

e. Vacuole

PLANT EMBRYOGENESIS, SHOOT APICAL MERISTEM (SAM), ROOT APICALMERISTEM

(RAM)

21. The first cell division in a plant zygote isasymmetrical.

a. True

b. False

22. At what stage of embryogenesis do PIN proteins firstinfluence orientation of the root-shoot

axis?

a. First cell division

b. Second cell division

c. 8-cell stage

d. Globular stage

e. Heart-shaped stage

23. Which hormone most strongly affects cell division inembryos?

a. IAA

b. GA

c. Ethylene

d. AA

e. CK

24. How do the major tissue systems in plants become establishedin developing embryo?

a. Anticlinal cell divisions

b. Periclinal cell divisions

c. All of the above

d. None of the above

STEM/ROOT PRIMARY, SECONDARY GROWTH

25. Fifteen years ago, your parent hung a swing from the lowerbranch of a tree in your yard. It is at the exact same height as itwas then. Why isn

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BIOLOGY 1A Lecture Notes - Lecture 28: Adult Stem Cell, Stem Cell, Unipotent

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