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MITOSIS-CELL DIVISION
• THIS IS A FINELY CONTROLLED
PROCESS THAT RESULTS IN TWO
IDENTICAL DAUGHTER CELLS. A
DIVIDING CELL:
– PRECISELY REPLICATES ITS DNA
– ALLOCATES THE TWO COPIES OF DNA
TO OPPOSITE ENDS OF THE CELL
– SEPARATES INTO TWO DAUGHTER
CELLS CONTAINING IDENTICAL DNA
SOMATIC CELLS
• MITOSIS IS THE PROCESS BY WHICH
ALL CELLS IN THE BODY (SOMATIC
CELLS) ARE MADE, EXCEPT FOR SEX
CELLS (GAMETES). THESE ARE
MADE THROUGH MEIOSIS, WHICH
WE WILL COVER IN THE NEXT
CHAPTER.
GENOME
• THE TOTAL HEREDITARY MAKE-UP
OF A CELL OF A PARTICULAR SPECIES
• GENOMES ARE ORGANIZED INTO
MULTIPLE FUNCTIONAL UNITES
CALLED CHROMOSOMES
CHROMOSOMES
• EACH CHROMOSOME CONSISTS OF
TWO SISTER CHROMATIDS. THE
TWO CHROMATIDS HAVE IDENTICAL
COPIES OF THE CHROMOSOME’S DNA
AND INITIALLY ATTACHED TO EACH
OTHER AT THE CENTROMERE
MITOSIS OVERVIEW
• 1) IN PREPARATION FOR DIVISION,
CHROMOSOMES AND ALL CELL
PARTS ARE DUPLICATED
• 2) DURING MITOSIS, SISTER
CHROMATIDS ARE PULLED APART,
ONE SET AT EACH END OF THE CELL
• 3) CYTOKINESIS IS THE DIVISION OF
THE CYTOPLASM INTO TWO
SEPARATE DAUGHTER CELLS
OVERVIEW VIDEO
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THE CELL CYCLE
• THE CELL CYCLE ALTERNATES
BETWEEN THE MITOTIC (M) PHASE,
OR DIVIDING PHASE, AND
INTERPHASE, THE NONDIVIDING
PHASE.
M PHASE
• THE SHORTEST PART OF THE CELL
CYCLE
• MITOSIS-DIVISION OF THE NUCLEUS
• CYTOKINESIS-DIVISION OF
CYTOPLASM
INTERPHASE
• THE NONDIVIDING PHASE, INCLUDES
MOST OF A CELL’S GROWTH AND
METABOLIC ACTIVITIES
– ABOUT 90% OF CELL CYCLE
– INTENSE BIOCHEMICAL ACTIVITY;
COPYING OF CHROMOSOMES AND
ALL ORGANELLES
– CONSISTS OF THREE PERIODS: G1, S,
G2
THE CELL CYCLE
INTERPHASE
• G1= FIRST GROWTH
• S = SYNTHESIS PHASE OCCURS WHEN DNA
IS MADE AS CHROMOSOMES ARE
DUPLICATED
• G2 = SECOND GROWTH PHASE
G2 PHASE
LATE INTERPHASE
• A G2 CELL SHOWS:
– A WELL DEFINED NUCLEUS WITH
NUCLEAR ENVELOPE
– ONE OR MORE NUCLEOLI
– TWO CENTROSOMES
– A PAIR OF CENTRIOLES IN EACH
CENTROSOME (ANIMAL CELLS ONLY)
– ASTERS AROUND CENTRIOLES
– DUPLICATED CHROMOSOMES ARE
LOOSELY PACKED CHROMATIN FIBERS
LATE INTERPHASE VIDEO
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PROPHASE
• IN THE NUCLEUS
– NUCLEOLI DISAPPEAR
– CHROMATIN FIBERS CONDENSE
IN THE CYTOPLASM
-MITOTIC SPINDLE FORMS; IT IS MADE
OF MICROTUBULES
-CENTROSOMES MOVE APART, MOVED
ALONG THE NUCLEAR SURFACE BY
LENGTHENING OF THE MICROTUBULE
BUNDLES
PROPHASE VIDEO
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PROMETAPHASE
• NUCLEAR ENVELOPE FRAGMENTS;
THIS ALLOWS MICROTUBULES TO
INTERACT WITH CHROMOSOMES
• SPINDLE FIBERS EXTEND FROM
EACH POLE TOWARDS THE MIDDLE
• EACH CHROMATID NOW HAS A
SPECIALIZED STRUCTURE, THE
KINTECHORE, LOCATED AT THE
CENTROMERE REGION
PROMETAPHASE
• KINETOCHORE MICROTUBULES
BECOME ATTACHED TO
KINETOCHORES AND PUT THE
CHROMOSOMES INTO MOTION
• OTHER MICROTUBULES RADIATE
FROM EACH CENTROSOME TOWARD
THE METAPHASE PLATE; THEY DO
NOT ATTACH TO CHROMOSOMES
PROMETAPHASE VIDEO
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METAPHASE
• CENTROSOMES ARE AT OPPOSITE POLES
OF THE CELL
• CHROMOSOMES MOVE TO THE
METAPHASE PLATE, MIDDLE OF SPINDLE
POLES
• CENTROMERES ARE ALIGNED ON THE
METAPHASE PLATE
• KINETOCHORES OF SISTER CHROMATIDS
FACE OPPOSITE POLES, SO IDENTICAL
CHROMATIDS ARE ATTACHED TO FIBERS
FROM OPPOSITE ENDS OF PARENT CELL
METAPHASE VIDEO
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ANAPHASE
• SISTER CHROMATIDS SPLIT APART
INTO SEPARATE CHROMOSOMES AND
MOVE TO OPPOSITE POLES
• CHROMOSOMES MOVE
CENTROMERE FIRST IN A “V” SHAPE
DUE TO KINETOCHORE FIBER
ATTACHMENT TO CENTROMERES
• KINETOCHORE MICROTUBULES
SHORTEN
• THE POLES OF THE CELL MOVE
FARTHER APART, ELONGATING THE
CELL
ANAPHASE VIDEO
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TELOPHASE
• NONKINETOCHORE MICROTUBULES
FURTHER ELONGATE THE CELL
• DAUGHTER NUCLEI BEGIN TO FORM
• NUCLEAR ENVELOPES FORM AROUND
THE CHROMOSOMES (FROM FRAGMENTS
OF THE PARENT CELL’S NUCLEAR
ENVELOPE)
• NUCLEOLI REAPPEAR
• CHROMATIN FIBER OF EACH
CHROMOSOME UNCOILS AND
CHROMOSOMES BECOME LESS DISTINCT
TELOPHASE VIDEO
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CYTOKINESIS
• MITOSIS, THE EQUAL DIVISION OF
ONE NUCLEUS INTO TWO
GENETICALLY IDENTICAL NUCLEI IS
COMPLETE
• CYTOKINESIS, THE PINCHING OF THE
CYTOPLASM FORMING A CLEAVAGE
FURROW, AND FINALLY THE
APPEARANCE OF TWO SEPARATE
CELLS
• PLANT CELLS: FORM A CELL PLATE
BETWEEN CELLS
CYTOKINESIS VIDEO
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BACTERIA
BINARY FISSION
• PROKAROTES REPRODUCE BY BINARY FISSION,
WHICH MAY BE THE EVOLUTIONARY
PRECURSOR TO MITOSIS
– THE CHROMOSOME IS REPLICATED AND REMAINS
ATTACHED TO MEMBRANE
– BETWEEN ATTACHMENT SITES, THE MEMBRANE GROS
AND SEPARATES THE TWO COPIES OF CHROMOSOMES
– THE BACTERIA GROWS TO TWICE ITS SIZE AND
MEMBRANE PINCHES INWARD
– A CELL WALL FORMS ACROSS THE BACTERIUM
BETWEEN THE TWO CHROMOSOMES
BINARY FISSION
REGULATION OF THE
CELL CYCLE
• NORMAL GROWTH, DEVLOPMENT
AND MAINTENANCE DEPEND ON THE
TIMING AND RATE OF MITOSIS. CELL
TYPES DIFFER IN THEIR PATTERNS
OF DIVISION:
– HUMAN SKIN CELLS DIVIDE OFTEN
– LIVER CELLS ONLY DIVIDE WHEN
NEEDED, AS IN WOUND REPAIR
– NERVE AND MUSCLE CELLS TO NOT
DIVIDE IN MATURE HUMANS
THE CELL CYCLE
CONTROL SYSTEM
• THIS IS A MOLECULAR CLOCK AND A
SET OF CHECKPOINTS, THAT
ENSURE THAT CONDITIONS ARE MET
BEFORE CYCLE ADVANCES.
MALFUNCTIONS IN SYSTEM CAN
RESULT IN CANCER
THE CHECKPOINTS
(G1, G2, AND M PHASES)
• SIGNALS AT CHECKPOINTS REPORT
STATUS OF CELL CONDITIONS (e.g.,
FAVORABLE ENVIRONMENT?, CELL
BIG ENOUGH?, DNA COPIED?)
• CHECKPOINTS INTEGRATE
INTRACELLULAR AND
EXTRACELLULAR INFORMATION
• G1 CHECKPOINT MOST IMPORTANT:
KNOWN AS THE “RESTRICTION
POINT”
G1 CHECKPOINT
• A GO-AHEAD SIGNAL INDICATES
THAT CELL WILL COMPLETE CYCLE
• IN ABSENCE OF GO-AHEAD, THE
CELL MAY EXIT THE CELL CYCLE,
SWITCHING TO NONDIVIDING STATE
CALLED THE G0 PHASE
• MANY CELLS OF HUMAN BODY ARE
IN G0, (MUSCLE, NERVE, AND LIVER)
CELL CYCLE CHECKPOINTS
CELL CYCLE
CONTROLLED BY
PROTEIN KINASES
• PROTEIN KINASES ARE ENZYMES THAT
CATALYZE THE TRANSFER OF A
PHOSPHATE FROM ATP TO TARGET
PROTEIN
• PHOSPHORYLATION INDUCES A
CONFORMATIONAL CHANGE THAT EITHER
ACTIVATES OR INACTIVATES A TARGET
PROTEIN
• CHANGES IN TARGET PROTEIN AFFECT
THE PROGESSION THROUGH CELL CYCLE
CYCLINS: CONTROL
KINASE ACTIVITY
• THESE REGULATORY PROTEINS ARE
NAMED CYCLINS, BECAUSE THEIR
CONCENTRATIONS CHANGE
THROUGHOUT THE CELL CYCLE
• PROTEIN KINASES THAT REGULATE
CELL CYCLE ARE CYCLINDEPENDENT KINASES (Cdks), AND
ARE ONLY ACTIVE WHEN ATTACHED
TO A CYCLIN
MPF: A CYCLIN-CDK
COMPLEX
• MPF: MATURATION PROMOTING
FACTOR
• CYCLIN’S CHANGES IN
CONCENTRATION REGULATES MPF
ACTIVITY, WHICH ACTS AS A
MITOTIC CLOCK THAT REGULATES
CHANGES IN THE DIVIDING CELL
MPF: THE PROCESS
• CYCLIN IS PRODUCED AT A UNIFORM
RATE THROUGHOUT CELL CYCLE, AND
ACCUMULATE DURING INTERPHASE
• CYCLIN COMBINES WITH CDK TO FORM
ACTIVE MPF, WHICH REGULATES MPF
CONCENTRATIONS
• MPF PHOSPHORYLATES PROTEINS THAT
PARTICIPATE IN MITOSIS AND INITIATES:
– CHROMOSOME CONDENSATION DURING
PROPHASE
– NUCLEAR ENVELOPE FRAGMENTATION
DURING PROMETAPHSE
MPF-CYCLIN ACTIVITY
FACTORS AFFECTING
CELL DIVISION
• CHEMICAL: GROWTH FACTORS
NEEDED FOR CELL DIVISION
• PHYSICAL: CROWDING INHIBITS
CELL DIVISION; ALSO, MOST ANIMAL
CELLS MUST ADHERE TO A SURFACE,
WITHOUT WHICH CELL CYCLE IS
SIGNALED TO STOP
DENSITY-DEPENDENT
INHIBITION
CANCER CELLS
• CANCER CELLS DO NOT STOP
GROWING IN RESPONSE TO CELL
DENSITY
• CANCER CELLS MAY MAKE GROWTH
FACTORS THEMSELVES
• THEY MAY HAVE AN ABNORMAL
GROWTH FACTOR SIGNALING
SYSTEM
• THEY CONTINUE TO DIVIDE
INDEFINITELY, AS LONG AS
NUTRIENTS ARE AVAILABLE
CANCER
• TUMOR = AN UNREGULATED
GROWING MASS OF CELLS
• MALIGNANCY- TUMOR THAT IS
INVASIVE ENOUGH TO IMPAIR
NORMAL FUNCTION OF ONE OR
MORE ORGANS
• METASTASIS - MIGRATING CANCER
CELLS INVADE OTHER PARTS OF
BODY AWAY FROM ORIGINAL SITE
METASTASIS