agenda 11/1/11 check ch. 11&12 notes/sq finish cell cycle, regulation and cancer (also...

Agenda 11/1/11

• Check Ch. 11&12 Notes/SQ• Finish cell cycle, regulation and cancer (also apoptosis)• Preview lab 3 -

http://www.phschool.com/science/biology_place/labbench/lab3/intro.html

Homework –Prelab Lab 3 worksheet ( used to do: for each part (3A1, 3A2, 3B1,

3B2) write purpose, what you will be observing, and what you will be analyzing – then do the lab bench activity as practice!!

Ch. 13 notes and self-quiz due Friday and Ch. 47 Animal Development (hard chapter!!) notes due Monday 11/7

Quiz on cell signaling, mitosis/meiosis and development next Tuesday 11/8



• The mitotic (M) phase of the cell cycle alternates with the much longer interphase.– The M phase includes mitosis and cytokinesis.– Interphase accounts

for 90% of the cell cycle.

1. The Cell Cycle

Copyright © 2002 Pearson Education, Inc., publishing as Benjamin Cummings

Fig. 12.4

Let’s watch an animation – online lesson 4.1 – Activity 2


Fig. 12.5 left


Fig. 12.5 right

• Assembly of the spindle microtubules starts in the centrosome.– The centrosome (microtubule-organizing

center) of animals has a pair of centrioles at the center, but the function of the centrioles is somewhat undefined.


Fig. 12.6a

• When a chromosome’s kinetochore is “captured” by microtubules, the chromosome moves toward the pole from which those microtubules come.

• When microtubules attach to the other pole, this movement stops and a tug-of-war ensues.

• Eventually, the chromosome settles midway between the two poles of the cell, the metaphase plate.


• One hypothesis for the movement of chromosomes in anaphase is that motor proteins at the kinetochore “walk” the attached chromosome along the microtubule toward the opposite pole.– The excess microtubule sections

depolymerize.


Fig. 12.7a

• Nonkinetichore microtubules are responsible for lengthening the cell along the axis defined by the poles.– These microtubules interdigitate across the

metaphase plate.– During anaphase motor proteins push

microtubules from opposite sides away from each other.

– At the same time, the addition of new tubulin monomers extends their length.


• On the cytoplasmic side of the cleavage furrow a contractile ring of actin microfilaments and the motor protein myosin form.

• Contraction of the ring pinches the cell in two.


Fig. 12.8a

• Cytokinesis in plants, which have cell walls, involves a completely different mechanism.

• During telophase, vesicles from the Golgi coalesce at the metaphase plate, forming a cell plate.– The plate enlarges until its

membranes fuse with the plasma membrane at the perimeter, with the contents of the vesicles forming new wall material in between.


Fig. 12.8b


Fig. 12.9

• Prokaryotes reproduce by binary fission, not mitosis.

• Possible intermediate evolutionary steps are seen in the division of two types of unicellular algae.

4. Mitosis in eukaryotes may have evolved

from binary fission in bacteria

• The distinct events of the cell cycle are directed by a distinct cell cycle control system.– These molecules trigger and coordinate key

events in the cell cycle. – The control cycle has

a built-in clock, but it is also regulated by external adjustments and internal controls.


Fig. 12.13

• Cyclin levels rise sharply throughout interphase, then fall abruptly during mitosis.

• Peaks in the activity of one cyclin-Cdk complex, MPF, correspond to peaks in cyclin concentration.


Fig. 12.14a

The M phase checkpoint • Ensures all chromosomes properly attached to

spindle at metaphase plate before anaphase– This ensures that daughter cells do not end up with

missing or extra chromosomes.

• A protein signal to delay anaphase originates at kinetochores that have not yet attached to spindle microtubules.– This keeps the anaphase-promoting complex (APC) in

an inactive state.– When all kinetochores are attached, the APC activates,

triggering breakdown of cyclin and inactivation of proteins uniting sister chromatids together.


• All necessary nutrients must be present for cell division and usually growth factor also.– For example, platelet-derived growth factors

(PDGF), produced by platelet blood cells, bind to tyrosine-kinase receptors of fibroblasts, a type of connective tissue cell.

– This triggers a signal-transduction pathway that leads to cell division.

• In a living organism, platelets release PDGF in the vicinity of an injury.

• The resulting proliferation of fibroblasts help heal the wound.


• The role of PDGF is easily seen in cell culture.– Fibroblasts in culture will only divide in the

presence of medium that also contains PDGF.


Fig. 12.15

• Growth factors appear to be a key in density-dependent inhibition of cell division.– Cultured cells normally

divide until they form a single layer on the inner surface of the culture container.

– If a gap is created, the cells will grow to fill the gap.

– At high densities, the amount of growth factors and nutrients is insuffi-cient to allow continued cell growth.


Fig. 12.16a

• Most animal cells also exhibit anchorage dependence for cell division.– To divide they must be anchored to a

substratum, typically the extracellular matrix of a tissue.

• Cancer cells are free of both density-dependent inhibition and anchorage dependence.


Fig. 12.16b

• Cancer cells divide excessively and invade other tissues because they are free of the body’s control mechanisms. – Cancer cells do not stop dividing when growth

factors are depleted either because they manufacture their own, have an abnormality in the signaling pathway, or have a problem in the cell cycle control system.

3. Cancer cells have escaped from cell cycle controls


• Cancer cells may divide indefinitely if they have a continual supply of nutrients.– In contrast, nearly all mammalian cells divide

20 to 50 times under culture conditions before they stop, age, and die.

– Cancer cells may be “immortal”.• Cells (HeLa) from a tumor removed from a woman

(Henrietta Lacks) in 1951 are still reproducing in culture.


• The abnormal behavior of cancer cells begins when a single cell in a tissue undergoes a transformation that converts it from a normal cell to a cancer cell.– Normally, the immune system recognizes and destroys

transformed cells.– However, cells that evade destruction proliferate to

form a tumor, a mass of abnormal cells.

• If the abnormal cells remain at the originating site, the lump is called a benign tumor. – Most do not cause serious problems and can be

removed by surgery.


• In a malignant tumor, the cells leave the original site to impair the functions of one or more organs.– This is what you think of as “cancer”– These cancer cells often lose attachment to

nearby cells, are carried by the blood and lymph system to other tissues, and start more tumors in a event called metastasis.



Fig. 12.17

• Treatments for metastasizing cancers include high-energy radiation and chemotherapy with toxic drugs.– These treatments target actively dividing cells.

• Researchers are beginning to understand how a normal cell is transformed into a cancer cell.– The causes are diverse.– However, cellular transformation always

involves the alteration of genes that influence the cell cycle control system.


Apoptosis

• Cell suicide for the good of the body –

• Cell signaling pathways to turn on enzymes to digest the cell and implode

Lab 3

• Lab bench

• http://www.phschool.com/science/biology_place/labbench/lab3/intro.html




Agenda 11/2/11• Briefly go over prelab• AP Lab 3 - Part 3A1 and 3A2

– I will check prelabs while you are working

Homework – • Do analysis questions for 3A1 and 3A2• Ch. 13 notes and self-quiz due Friday and Ch. 47 Animal

Development (hard chapter!!) notes due Monday 11/7• Quiz on cell signaling, mitosis/meiosis and development next

Tuesday 11/8

Agenda 11/3/11• Discuss 3A analyses (10 min)

Let’s watch an animation – online lesson 4.1 – Activity 5• AP Lab 3 part 3B1 –meiosis simulation

Last 10 minutes Watch Lab Bench Sordaria part

• http://www.phschool.com/science/biology_place/labbench/lab3/intro.html

Homework – • Do analysis questions for 3B1• Ch. 13 notes and self-quiz due Friday and Ch. 47 Animal

Development (hard chapter!!) notes due Monday 11/7 • Quiz on cell signaling, mitosis/meiosis and development next

Tuesday 11/8

Me – book computer lab for Drosophila on 11/16



Agenda 11/4/11

• Do AP Lab 3 part 3B2• Go over analysis questions for all lab 3• Wrap up meiosis/Ch.13 (won’t get to this until next

Tuesday)Homework - • Ch. 47 Animal Development (hard chapter!!) notes due

Monday 11/7 (will check with Ch. 13) – use the week 12 Powerpoint online slides 2-37 as a guide as to what to focus on in the reading

• Quiz on cell signaling, mitosis/meiosis and development next Tuesday 11/8

• In humans, each somatic cell (all cells other than sperm or ovum) has 46 chromosomes.– Each chromosome can be distinguished by its size,

position of the centromere, and by pattern of staining with certain dyes.

• A karyotype display of the 46 chromosomes shows 23 pairs of chromosomes, each pair with the same length, centromere position, and staining pattern.

• These homologous chromosome pairs carry genes that control the same inherited characters.

1. Fertilization and meiosis alternate in sexual life cycles

• Karyotypes, ordered displays of an individual’s chromosomes, are often prepared with lymphocytes.

Fig. 13.3

• Fertilization restores the diploid condition by combining two haploid sets of chromosomes.

• Fertilization and meiosis alternate in sexual life cycles.

Fig. 13.4

3 Types of Life Cycles

• Meiosis reduces chromosome number by copying the chromosomes once, but dividing twice.

• The first division, meiosis I, separates homologous chromosomes.

• The second, meiosis II, separates sister chromatids.

Fig. 13.6

• Three events, unique to meiosis, occur during the first division cycle.

1. During prophase I, homologous chromosomes pair up in a process called synapsis.– A protein zipper, the synaptonemal complex, holds

homologous chromosomes together tightly.– Later in prophase I, the joined homologous

chromosomes are visible as a tetrad.– At X-shaped regions called chiasmata, sections of

nonsister chromatids are exchanged.– Chiasmata is the physical manifestation of crossing

over, a form of genetic rearrangement.

2. At metaphase I homologous pairs of chromosomes, not individual chromosomes are aligned along the metaphase plate.

• In humans, you would see 23 tetrads.

3. At anaphase I, it is homologous chromosomes, not sister chromatids, that separate and are carried to opposite poles of the cell.– Sister chromatids remain attached at the

centromere until anaphase II.

• The processes during the second meiotic division are virtually identical to those of mitosis.

• Mitosis produces two identical daughter cells, but meiosis produces 4 very different cells.

Fig. 13.8

Fig. 13.8

Three mechanisms of genetic variation

• 1) Independent Assortment

•For humans with n = 23, there are 223 or about 8 million possible combinations of chromosomes.

2) Crossing over • produces recombinant

chromosomes which combine genes inherited from each parent.

Fig. 13.10

• 3) Fertilization – The random nature of fertilization adds to the

genetic variation arising from meiosis.– Any sperm can fuse with any egg.

• An ovum is one of approximately 8 million possible chromosome combinations (actually 223).

• The successful sperm represents one of 8 million different possibilities (actually 223).

– The resulting zygote is composed of 1 in 70 trillion (223 x 223) possible combinations of chromosomes.

– Crossing over adds even more variation to this.

Sex and mutations are two sources of the continual generation of new genetic variability.

• Darwin recognized the importance of genetic variation in evolution via natural selection.

• A population evolves through the differential reproductive success of its variant members.

• Those individuals best suited to the local environment leave the most offspring, transmitting their genes in the process.

• This natural selection results in adaptation (the accumulation of favorable genetic variations) as the environment changes.

Evolutionary adaptation depends on a population’s genetic variation

agenda 11/1/11 check ch. 11&12 notes/sq finish cell cycle, regulation and cancer (also...

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