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Cell Cycle, Mitosis, Meiosis Cell Cycle, Mitosis, Meiosis

Cell Cycle, Mitosis, Meiosis - PowerPoint Presentation

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Cell Cycle, Mitosis, Meiosis - PPT Presentation

Unit 5 Welcome Back Musical Chairs TODAY Notes on Cell Cycle Become medical school students on oncology rotation Homework for next time Watch Bozeman video on cell cycle mitosis and meiosis There may be a quiz ID: 482806

cycle cell mitosis amp cell cycle amp mitosis cells growth cancer division control signals dna checkpoint phase cyclin divide

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Slide1

Cell Cycle, Mitosis, Meiosis

Unit 5Slide2

Welcome Back!

Musical Chairs

TODAY:

Notes on Cell Cycle

Become medical school students on oncology

rotation

Homework for next time: Watch Bozeman video on cell cycle, mitosis and meiosis. There *may* be a quiz.Slide3

Unit 5 Plan

AP Biology Essential Knowledge covered:

In

eukaryotes, heritable information is passed to the next generation via processes that include the cell cycle and mitosis or meiosis plus fertilization

.

Day 1 – Cell Cycle & Case Study

Day 2 – Mitosis & Case Study

Day 3 – Meiosis & Modeling Activity

Day 4 – Modeling continued, Quiz over notes/

Quizlet

(online)Slide4

Why Care about Cell Cycle Control?

Lifetime Risk of Developing Cancer: Approximately

_____

percent of men and women will be diagnosed with all cancer sites at some point during their

lifetime?

In

2012, there were an estimated 

__________ people living with all cancer sites in the United States.Slide5

Why Care about Cell Cycle Control?

Lifetime Risk of Developing Cancer: Approximately

39.6

percent of men and women will be diagnosed with all cancer sites at some point during their

lifetime?

In

2012, there were an estimated 13, 780,000

 people living with all cancer sites in the United States.Slide6

Why Care about Cell Cycle Control?

Oncologists – Study cancer

and help those affected

Average salary in 2015 ~ $277,000

Time to become an oncologist?

10-13 years

Bachelors, Medical School, Residency

Demand

?

United States will likely face a

48% increase in demand for oncologist services by 2020—in large part because of the expected 81% increase in cancer survivorship and the 48% increase in cancerincidence caused by the aging of the population. Slide7

Day 1 –

Cell Cycle

In eukaryotes,

heritable information

is passed to the next generation via processes that include the cell cycle and mitosis or meiosis plus fertilization

.

So, passing on heritable information begins with the ability for cells to go through the cell cycle.

Why else is the cell cycle important?Slide8

Some Cell Cycle Basics

The cell cycle is divided into Interphase and Mitotic (including mitosis & cytokinesis)

Interphase

consists of three phases: growth, synthesis of DNA, preparation for mitosis

.

Mitosis consists of prophase, metaphase, anaphase and telophase.

Mitosis alternates with interphase in the cell cycle.

Mitotic PhaseSlide9

Cell division results in genetically identical cellsSlide10

How

do cells know when to divide

?

C

ell communication

signals

chemical signals in cytoplasm give cue

signals usually are

proteins

activators

inhibitors

Activation of cell divisionSlide11

Coordination of cell division

A multicellular organism needs to coordinate cell division across different tissues & organs

critical for normal growth,

development & maintenance

Do you think cells all have

the same timing for their

cell cycle?

Discuss with a friend –

think of an example.Slide12

G

2

S

G

1

M

metaphase

prophase

anaphase

telophase

interphase (G

1

, S, G

2

phases)

mitosis (M)

cytokinesis (C)

C

Frequency of cell division varies by cell type

embryo

cell cycle < 20 minute

skin cells

divide frequently throughout life

12-24 hours cycle

liver cells

retain ability to divide, but keep it in reserve

divide once every year or two

mature nerve cells & muscle cells

do not divide at all after maturity

permanently in G

0

Frequency of cell divisionSlide13

Cell Cycle –

Think/Pair/Share

The cell cycle is a complex set of stages that is

highly regulated

with

checkpoints

, which determine the ultimate fate of the cell.

Why would it need to be highly regulated? What might the checkpoints result in?Slide14

Overview of Cell Cycle Control

Two

irreversible points

in cell cycle

replication of genetic material

separation of sister chromatids

Checkpoints

process is assessed & possibly halted

centromere

sister chromatids

single-stranded

chromosomes

double-stranded

chromosomes

There

s no

turning back,

now

!

Slide15

Checkpoint control system

Checkpoints

cell cycle controlled by

STOP

&

GO

chemical signals at critical points

signals indicate if key cellular

processes have been

completed correctly

3 major checkpoints:

G

1

, G

2

and MSlide16

Checkpoint control system

3 major checkpoints

:

G

1

can DNA synthesis begin?

G

2

has DNA synthesis been completed correctly?

commitment to mitosis

M

are all chromosomes attached to spindle?

can sister chromatids separate correctly?Slide17

G

1

Checkpoint is

the

most critical!

primary decision point

restriction point

if cell receives a

“GO-

ahead”signal

, it will

divide

if cell does

not

receive

signal, it exits cycle &

switches to

G

0

phaseSlide18

G

0

phase

G

0

phase

non-dividing, differentiated state

many human cells in G

0

phase

liver cells

in G

0

, but can be “called back” to cell cycle by external cues

nerve & muscle cells

highly specialized

arrested in G

0

& can never divideSlide19

“Go-ahead”

signals

Protein molecules that promote cell growth & division

internal signals

promoting factors

external signals

growth factors

Primary mechanism of control

phosphorylation

Use of

kinase

enzymes

Which either activates or inactivates cell signals by adding a phosphateSlide20

Cell cycle

Chemical

signals

Cyclins

(PROTEIN)

regulatory proteins

levels cycle in the

cell

Cdk’s

(ENZYME)

cyclin

-dependent kinases

phosphorylates cellular proteins

activates or inactivates proteins

Cdk-cyclin

complex

Forms

MPF (mitosis promoting factor)

complex

Triggers movement into next phase

activated Cdk

inactivated

CdkSlide21

Cdk / G

1

cyclin

Cdk / G

2

cyclin (MPF)

G

2

S

G

1

C

M

G

2

checkpoint

G

1

checkpoint

Active

Inactive

Active

Inactive

Inactive

Active

mitosis

cytokinesis

MPF

= Mitosis Promoting Factor

Replication completed

DNA integrity

Chromosomes attached at metaphase plate

M checkpoint

Growth factors

Nutritional state of cell

Size of cellSlide22

Cyclin

&

Cyclin

-dependent

kinases (

Cdk’s

)

CDKs &

cyclin

drive cell from

one phase to next in cell cycle

proper regulation of cell cycle is so key to life that the

genes for these regulatory proteins have been highly conserved

through

evolution

the genes are basically the same in yeast, insects, plants & animals (including humans)Slide23

External signals

Sometimes the signals are EXTERNAL…

Growth

factors

Proteins or steroid hormones

that bind to 

receptors

 on the cell surface, with the primary result of activating cellular proliferation

and/or

differentiation

.

Many growth factors are quite versatile, stimulating cellular division in numerous different cell types; while others are specific to a particular cell-type

Allow coordination

between cells

density-dependent

inhibition

crowded cells stop dividing

When not enough growth factor left to trigger division in any one cell, division stops

anchorage dependence

to divide cells must be attached to a substrate or tissue matrix

“touch sensor” receptorsSlide24

Cancer & Cell Growth

Cancer is essentially a failure

of cell division

control

unrestrained, uncontrolled cell growth

What control is lost?

lose checkpoint

stops

gene

p53

plays a key role in G

1

restriction point

p53 protein halts cell division if it detects damaged DNA

options:

stimulates repair enzymes to fix DNA

forces cell into G

0

resting stage

keeps cell in G

1

arrest

causes apoptosis of damaged cell

ALL

cancers have to shut down p53 activity

p53 is the

Cell Cycle

EnforcerSlide25

Development of Cancer

Cancer

develops only after a cell experiences ~6 key

mutations

(“hits”)

unlimited growth

turn

on

growth promoter genes

ignore checkpoints

turn

off tumor suppressor genes (p53)

escape apoptosis

turn

off

suicide genes

immortality = unlimited divisions

turn

on

chromosome maintenance genes

promotes blood vessel growth

turn

on

blood vessel growth genes

overcome anchor & density dependence

turn

off

touch-sensor gene

It

s like an

out of control

car

!Slide26

What causes these “hits”?

Mutations in cells can be triggered by

UV radiation

chemical exposure

radiation exposure

heat

cigarette smoke

pollution

age

geneticsSlide27

Tumors

Mass of abnormal cells

Benign tumor

abnormal cells remain at original site as a lump

p53 has halted cell divisions

most do not cause serious problems &

can be removed by surgery

Malignant tumors

cells leave original site

carried

by blood & lymph system to other tissues

start more tumors =

metastasis

impair functions of organs throughout bodySlide28

Traditional treatments for cancers

Treatments target rapidly dividing cells

high-energy radiation

kills rapidly dividing cells

chemotherapy

stop DNA replication

stop mitosis & cytokinesis

stop blood vessel growthSlide29

Time for your

oncology rotation!

You are medical school students on an oncology rotation

Choose a narrator, scribe and

researcher

Start with the “Mystery” – when you have answered the questions, raise a hand for your supervisor to check in with you (yes, that is me)

You must check in with me before proceeding to each new portion of your case study.

Your group’s grades will be based on our discussions – everyone must be prepared to answer the supervisors questions!