Reproduksi Sel-Mitosis Meiosis

8/10/2019 Reproduksi Sel-Mitosis Meiosis

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Mitosis & Meiosis


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The division of a unicellular organism reproduces

an entire organism, increasing the population.

Cell division on a larger scale can produce progeny

for some multicellular organisms.

This includes organisms

that can grow by cuttings

or by fission.

Cell d

ivision functions in reproduction,

growth, and repair

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

Fig. 12.1


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Cell division is also central to the development of

a multicellular organism that begins as a fertilized

egg or zygote. Multicellular organisms also use cell division to

repair and renew cells that die from normal wear

and tear or accidents.


Fig. 12.1b Fig. 12.1c


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Cell division requires the distribution of identical

genetic material - DNA - to two daughter cells.

What is remarkable is the fidelity with which DNA ispassed along, without dilution, from one generation

to the next.

A dividing cell duplicates its DNA, allocates the

two copies to opposite ends of the cell, and then

splits into two daughter cells.



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genome--A cells genetic information, packaged as

DNA

prokaryotes--often a single long DNA molecule.

eukaryotes--consists of several DNA molecules.

A human cell must duplicate about 3 m of DNA

and separate the two copies such that each

daughter cell ends up with a complete genome.

Cell division distributes identical sets of

chromosomes to daughter cells



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Each eukaryotic chromosome consists of a long,linear DNA molecule.

Each chromosome has hundreds or thousands ofgenes, the units that specify an organismsinherited traits.

Associated with DNA are proteins called

histones that maintain its structure and helpcontrol gene activity.

This DNA-protein complex, chromatin,is

organized into a long thin fiber.After the DNA duplication, chromatin

condenses, coiling and folding to make a smallerpackage.



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DNA is packaged as a chromosome


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Each duplicated chromosome consists of twosister chromatidswhich contain identical copiesof the chromosomes DNA.

As they condense, theregion where the strandsconnect shrinks. This

narrow area, is thecentromere.

Later, the sister

chromatids are pulledapart and repackagedinto two new nuclei atopposite ends of

the parent cell.Copyright 2002 Pearson Education, Inc., publishing as Benjamin CummingsFig. 12.3


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Why do cells divide?

The frequency of cell division varies with cell

type.

Some human cells divide frequently throughout life

(skin cells), others have the ability to divide, but keepit in reserve (liver cells), and mature nerve andmuscle cells do not appear to divide at all aftermaturity.

Cancer cells escape the controls that direct cell

division

Th i i h l i h


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The mitotic(M)phaseof the cell cycle alternateswith the much longer interphase.

The M phase includes mitosis and cytokinesis.

Interphase accountsfor 90% of the cell

cycle.

The mitotic phase alternates with

interphase in the cell cycle: an overview


Fig. 12.4


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During interphase the cell grows by producing

proteins and cytoplasmic organelles, copies its

chromosomes, and prepares for cell division. Interphase has three subphases:

the G1phase (first gap) centered on growth,

the S phase (synthesis) when DNA replicationoccurs thus the chromosomes are copied,

the G2phase (second gap) where the cell completes

preparations for cell division,

and divides (M).

The daughter cells may then repeat the cycle.



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Mitosis is a continuum of changes.

For description, mitosis is usually broken into five

subphases:

prophase

prometaphase

metaphase

anaphase telophase


FIVE PHASES


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Late Interphase

By late interphase, the

chromosomes have been

duplicated but are loosely

packed. The centrosomeshave

been duplicated and

begin to organize

microtubules into anaster (star).


CLICK TO VIEW ANIMATION.


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Prophase

The chromosomes are

tightly coiled, with sister

chromatids joined together.

The nucleoli disappear. The mitotic spindle begins

to form and appears to push

the centrosomes away

from each other toward

opposite ends (poles)

of the cell.




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Prometaphase

The nuclear envelope

fragments and microtubules

from the spindle interact

with the chromosomes. Microtubules from one

pole attach to one of two

kinetochores, special

regions of the centromere,while microtubules from

the other pole attach to

the other kinetochore.




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Metaphase

The spindle fibers push

the sister chromatids

until they are all arranged

at the metaphase plate,an imaginary plane

equidistant between the

poles, defining

metaphase.



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Anaphase

The centromeres divide,separating the sister

chromatids.

Each is now pulledtoward the pole to which

it is attached by spindle

fibers.

By the end, the two

poles have equivalent

collections of

chromosomes.



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Telophase

The cell continues to elongateas free spindle fibers from eachcentrosome push off eachother.

Two nuclei begin for form,surrounded by the fragmentsof the parents nuclearenvelope.

Chromatin becomes

less tightly coiled.

Cytokinesis, divisionof the cytoplasm,begins.



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Fig. 12.5 left


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Fig. 12.5 right


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Click for a time lapse movie of

ANIMAL mitosis



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More about that spindle apparatus

The mitotic spindle, fibers composed of

microtubules and associated proteins, is a major

driving force in mitosis.

As the spindle assembles during prophase, the

elements come from partial disassembly of the

cytoskeleton.

The spindle fibers elongate by incorporating more

subunits of the protein tubulin.



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Assembly of the spindle microtubules starts in

the centrosome.

The centrosome (microtubule-organizing center) ofanimals has a pair of centrioles at the center, but the

function of the centrioles is somewhat undefined.


Fig. 12.6a


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Each sister chromatid has a kinetochoreof

proteins and chromosomal DNA at the

centromere.The kinetochores of the joined sister chromatids

face in opposite directions.

During prometaphase,some spindle

microtubules

attach to the

kinetochores.


Fig. 12.6b


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When a chromosomes 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 midwaybetween the two poles of the cell, the

metaphase plate.

Other microtubules from opposite poles interactas well, elongating the cell.



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One hypothesis for the movement of

chromosomes in anaphase is that motor proteins

at the kinetochore walk the attachedchromosome along the microtubule toward the

opposite pole.

The excess microtubule sections depolymerize.


Fig. 12.7a


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Experiments

support the

hypothesis thatspindle fibers

shorten during

anaphase from the

end attached to the

chromosome, not

the centrosome.


Fig. 12.7b


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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.



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Cytokinesis, division ofthe cytoplasm, typically

follows mitosis.

In animals, the first signof cytokinesis (cleavage)

is the appearance of a

cleavage furrowin thecell surface near the old

metaphase plate.

Cytokinesis divides the cytoplasm


Fig. 12.8a


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On the cytoplasmic side

of the cleavage furrow a

contractile ring of actinmicrofilaments and the

motor protein myosin

form.

Contraction of the ring

pinches the cell in two.


Fig. 12.8a


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Cytokinesis

Once the nucleardivision has ended, thesecond stage of the Mphase begins

Cytokinesis is separatefrom mitosis [nucleardivision]

Cytokinesis divides thecytoplasm, divvies up theorganelles ANDcompletes the cellsdivision


Mi i i k h l d


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Prokaryotes reproduce by binary fission,notmitosis.

Most bacterial genes are located on a single bacterial

chromosomewhich consists of a circular DNAmolecule and associated proteins.

While bacteria do not have as many genes or DNA

molecules as long as those in eukaryotes, theircircular chromosome is still highly folded and

coiled in the cell.

Mitosis in eukaryotes may have evolved

from binary fission in bacteria


In binary fission chromosome


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Cell division involves

inward growth of the

plasma membrane,

dividing the parent cellinto two daughter cells,

each with a complete

genome.

Copyright 2002 Pearson Education, Inc., publishing as Benjamin CummingsFig. 12.10

In binary fission, chromosomereplication begins at one pointin the circular chromosome, the

origin of replicationsite.These copied regions begin to

move to opposite ends of thecell.


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It is quite a jump from

binary fission to

mitosis.

Possible intermediate

evolutionary steps are

seen in the division of

two types of unicellularalgae.

In dinoflagellates,

replicated chromosomes

are attached to thenuclear envelope.

In diatoms, the spindle

develops within the

nucleus.



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Chemical signals in the cytoplasm

control the cell cycle!

The cell cycle appears to be driven by specific

chemical signals in the cytoplasm.

Fusion of an S phase and a G1 phase cell, induces the G1

nucleus to start S phase.

Fusion of a cell in mitosis with one in interphase induces

the second cell to enter mitosis.


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The distinct events of the cell cycle are directed

by a distinct cell cycle control system.

These molecules trigger and coordinate key events inthe cell cycle.

The control cycle has

a built-in clock, but it

is also regulated byexternal adjustments

and internal controls.


Fig. 12.13

The G1 Checkpoint the restriction


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If the cells receives a go-ahead signal, it usually

completes the cell cycle and divides. If it does not receive a go-ahead signal, the cell exits

the cycle and switches to a nondividing state, the G0

phase.

Most human cells are in this phase.

Liver cells can be called back to the cell cycle by external

cues (growth factors), but highly specialized nerve and

muscle cells never divide.


The G1 Checkpoint, the restriction

point in mammalian cells is the most

important


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Rhythmic fluctuations in the abundance andactivity of control molecules pace the cell cycle.

Some molecules are protein kinases that activate or

deactivate other proteins by phosphorylating them.The levels of these kinases are present in constant

amounts, but these kinases require a second

protein, a cyclin, to become activated.

Level of cyclin proteins fluctuate cyclically.

The complex of kinases and cyclin forms cyclin-

dependent kinases(Cdks).


Cyclins activate kinases


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Control of the Cell Cycle



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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


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The M phase checkpoint ensures that all the

chromosomes are properly attached to the

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

missing or extra chromosomes.

A 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 andinactivation of proteins uniting sister chromatids

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

A i f l h i l d h i l


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A variety of external chemical and physicalfactors can influence cell division.

Particularly important for mammalian cells aregrowth factors, proteins released by one groupof cells that stimulate other cells to divide.

For example,platelet-derived growth factors (PDGF),

produced by platelet blood cells, bind to tyrosine-kinase receptors of fibroblasts, a type of connectivetissue cell.

This triggers a signal-transduction pathway that leads

to cell division. Each cell type probably responds specifically to a

certain growth factor or combination of factors.



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The role of PDGF is easily seen in cell culture.

Fibroblasts in culture will only divide in the presenceof medium that also contains PDGF.

Copyright 2002 Pearson Education, Inc., publishing as Benjamin CummingsFig. 12.15

f b k


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Growth factors appear to be a key in density-

dependent inhibitionof cell division.

Cultured cells normallydivide until they form asingle layer on the innersurface of the culturecontainer.

If a gap is created, thecells will grow to fillthe gap.

At high densities, theamount of growth factorsand nutrients is insuffi-cient to allow continuedcell growth.

Copyright 2002 Pearson Education, Inc., publishing as Benjamin CummingsFig. 12.16a

i l ll l hibi h


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Most animal cells also exhibit anchorage

dependencefor cell division.

To divide they must be anchored to a substratum,typically the extracellular matrix of a tissue.

Control appears to be mediated by connections

between the extracellular matrix and plasma membrane

proteins and cytoskeletal elements.

Cancer cells are free of both density-dependent

inhibition and anchorage dependence.


Fig. 12.16b

Cancer cells have escaped from cell


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Cancer cells divide excessively and invade othertissues because they are free of the bodys control

mechanisms.

Cancer cells do not stop dividing when growth factorsare depleted either because they manufacture their own,

have an abnormality in the signaling pathway, or have a

problem in the cell cycle control system.

If and when cancer cells stop dividing, they do so

at random points, not at the normal checkpoints in

the cell cycle.

Cancer cells have escaped from cellcycle controls


C ll di id i d fi i l if h h


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Cancer cell may divide indefinitely if they have a

continual supply of nutrients.

In contrast, nearly all mammalian cells divide 20 to 50times 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.


Th b l b h i f ll b i


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The abnormal behavior of cancer cells begins

when a single cell in a tissue undergoes a

transformationthat converts it from a normalcell 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.


I li h ll l h i i l


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In a malignant tumor, the cells leave the original

site to impair the functions of one or more

organs.This typically fits the colloquial definition of cancer.

In addition to chromosomal and metabolic

abnormalities, cancer cells often lose attachment to

nearby cells, are carried by the blood and lymphsystem to other tissues, and start more tumors in a

event called metastasis.



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Fig. 12.17

T f i i i l d


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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.



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Meiosis creates Genetic Diversity


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Purpose of Meiosis

To make haploid cells

When 2 haploid cells fuse; the diploid state is

restored.

You get 1 copy of each chromosome from each

parent. This is called a homologous pair.

This increases genetic diversity.

Karyotypes sort the chromosomes


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y ypinto homologous pairs

[22 + XX or XY]

C iti l diff b t it i


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Critical differences between mitosis

and meiosis

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.

Di ision in meiosis I occ rs in fo r phases


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Division in meiosis I occurs in four phases:

prophase, metaphase, anaphase, and telophase.

During the preceding interphase thechromosomes are replicated to form sister

chromatids.

In prophase I the chromosomes condense and


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In prophase I, the chromosomes condense and

homologous chromosomes pair up to form

tetrads. In a process called synapsis, special proteins attach

homologous chromosomes tightly together.

At several sites the chromatids of

homologous chromosomes arecrossed (chiasmata) and segments

of the chromosomes are traded.

A spindle forms from eachcentrosome and spindle fibers

attached to kinetochores on

the chromosomes begin to

move the tetrads around.


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Crossing Over


At metaphase I the tetrads are all arranged at the


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At metaphase I, the tetrads are all arranged at the

metaphase plate.

Microtubules from one pole are attached to thekinetochore of one chromosome of each tetrad,

while those from the other pole are attached to the

other.

In anaphase I,the homologous

chromosomes

separate andare pulled toward

opposite poles.


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In telophase I movement of homologous


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In telophase I, movement of homologous

chromosomes continues until there is a haploid

set at each pole.

Each chromosome consists of linked sister

chromatids.

Cytokinesis by the same

mechanisms as mitosis

usually occurs simultaneously.

In some species, nuclei

may reform, but there isno further replication

of chromosomes.


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The second meiotic division is

very similar to mitosis.

The 3 critical differences all occurin the first round of meiotic

divisions.

Three critical differencesall occur


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1. Prophase I--homologous chromosomes pair

up in a process called synapsis.

A protein zipper, the synaptonemal complex, holdshomologous 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.

Three critical differencesall occur

during Meiosis I

2 Metaphase I--homologous pairs of


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2. Metaphase I--homologous pairs of

chromosomes, not individual chromosomes are

aligned along the metaphase plate. In humans, you would see 23 tetrads.

3. 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 2 identical cells


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pwhile meiosis produces 4 haploid

and very different cells

Comparison Summary


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Comparison Summary

Worth MAJOR POINTS!

Independent assortment


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Independent assortment

alone would find each

individual chromosome in

a gamete that would be

exclusively maternal or

paternal in origin.

However, crossing over

produces recombinant

chromosomeswhich

combine genes inheritedfrom each parent.

The three sources of genetic variability in a


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T e t ee so ces o ge et c va ab ty asexually reproducing organism are:

Independent assortment of homologous

chromosomes during meiosis I and of nonidenticalsister chromatids during meiosis II.

Crossing over between homologous chromosomesduring prophase I.

Random fertilization of an ovum by a sperm.

All three mechanisms reshuffle the various genescarried by individual members of a population.

Mutations, still to be discussed, are whatultimately create a populations diversity of genes.

Oogenesis vs Spermatogenesis


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Oogenesis vs Spermatogenesis

Oogeneisisegg production

When a girl is born she is born with all her eggs suspended inmeiosis I. Each division of meiosis is uneven. At the end

you have 1 large cell that will be the released egg, and 3 polar

bodies that will disintegrate. Egg production will continue

once a month until the eggs are gone. Spermatogenesissperm production

Once puberty is reached, males continually produce

sperm at a rate of 10s of millions. All cells

produced as a result of meiosis will become sperm.

The human male can release 100 to 650 million

sperm with each ejaculation, and can ejaculate daily

with out losing fertilizing capicity.


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Animal Life Cycle


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Plant Life Cycle

Reproduksi Sel-Mitosis Meiosis

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