Transcript Complete and Incomplete Metamorphosis

Complete and
Incomplete
Metamorphosis
What is metamorphosis?
• Metamorphosis refers to the way
that certain organisms develop, grow,
and change form.
• Metamorphosis actually means
"change".
• Felt he was an outsider
– Jewish in Catholic Prague
– Sickly
– Lonely
• Perceived human beings as
being trapped by authority in
a hopeless world
• Became frustrated at having
to support his family
• Had to work in a meaningless
bureaucratic job where he was
just another pencil pusher
– Took time away from his writing
Franz Kafka
Two Types of Metamorphosis
• COMPLETE METAMORPHOSIS has FOUR stages.
• INCOMPLETE METAMORPHOSIS - has THREE stages (p.s.
incomplete doesn’t mean not finished. It just means
that the adult in complete metamorphosis is completely
different from the larva. A nymph and its adult form are
not completely different. They’re only a little different.)
4 STAGES OF
COMPLETE METAMORPHOSIS
• Egg
• Larva
• Pupa
• Adult
• EGG
• The female lays eggs.
• LARVA
• Larva hatch from the eggs. They do not look
like adult insects. They usually have a wormlike shape.
• Caterpillars(毛虫）, maggots (蛆虫）, and
grubs（蛴螬）are all just the larval stages of
insects. Larvae molt their skin several times
and they grow slightly larger.
• ADULT
• Inside the cocoon, the larvae change
into adults. After a period of time, the
adult breaks out of the cocoon.
INCOMPLETE METAMORPHOSIS
Let’s take a closer look
at each stage!
3 STAGES OF
INCOMPLETE METAMORPHOSIS
• Egg
• Nymph
• Adult
• EGG
• A female insect lays eggs. These
eggs are often covered by an egg
case which protects the eggs and
holds them together.
• NYMPH
• The eggs hatch into nymphs.
• Nymphs looks like small adults, but usually don't have
wings.
• Insect nymphs eat the same food that the adult insect eats.
• Nymphs shed or molt their exoskeletons (outer casings
made up of a hard substance called chitin) and replace
them with larger ones several times as they grow.
• Most nymphs molt 4-8 times.
• ADULT
• The insects stop molting when they
reach their adult size. By this time,
they have also grown wings.
ENDOCRINE- describing or relating to any gland or
other group of cells that synthesizes hormones and
secretes them directly into the blood, lymph, or other
intercellular fluid
Endocrine cells release
protein and non-protein
hormones
Synthesis of hormones is
orchestrated by the CNS
Hormones effects are
tissue dependent
Hormonal Control of Insect Metamorphosis
Temperature,
Light, Stress,
etc.
Prothoracicotropic促前
胸腺hormone (PTTH)
Brain
Corpus Allatum咽侧体Prothoracic Gland前胸腺
Juvenile
Hormone (JH)保
幼激素
Larva
Pupa
Ecdysteroid蜕皮
激素
Adult
Control of Metamorphosis by Internal and External
Factors
Temperature,
Light, Stress,
etc.
Brain
Temperature (day degrees)
Critical size matched (availability of food)
Light (photoperiod)
Chemicals
Amount of moisture（湿度）
Stress: mutagens, predators（肉食者）, etc.
Ecdysone: “Molting Hormone”
Steroid hormone produced by prothoracic gland (lipid soluble,
passes through cell membrane to the nucleus)
Activates early response genes (TFs) and then late response genes
(may cause differentiation,cell proliferation and migration, structural
changes, apoptosis)
Primes insect to respond to second hormone, EH
Ec
Early Response:
Transcription
Factors
USP
Binding Site
Late Response:
Transcription initiated
by Transcription
Factors
Chromosome Puffing in Flies
Observed in giant salivary gland chromosomes
(no cell division after replication)
Can be inhibited by actinomycin(放线菌素D）
Puffing is where transcription is occurring.
Ecdysone can be detected by fluorescent
antibodies localized to the puffing
Early puffs and late puffs seen in larva to pupa
and pupa to adult molt
Alternative Splicing of Ecdysone Receptor PremRNA Creates Several Forms of the EcReceptor Allowing Cell Type Specific Ecdysone
Response
Regulation of JH Levels
Amount of Hormone
Juvenile Hormone
Ecdysone
Larva
Pupa
Adult
Low = larva stage; Medium JH levels = pupa stage; No JH = adult stage
Rate of release limited by synthesis
Amounts of JH also regulated by protein degradation and
methyltransferase levels (can be protected by JH binding proteins,
degraded by JH esterase)
Metamorphosis in Action: Remember Imaginal Discs?
Adult Insect: - JH
Immature Insect: + JH
Insect control by targeting
metamorphosis
Juvenile hormone mimic: Keep insects in larval stage
-- Effective control for insects such as
mosquitoes
Juvenile hormone antagonist: Cause death of larva or early
metamorphosis
-- Effective control for crop pests such as hornworm
Genes for juvenile hormone binding hormone and JH esterase have been
identified
Frogs: Tadpole to Adult
Hormonal Control of Frog
Metamorphosis
Secretions of two hormones, thyroxine (T4) and triiodothyronine (T3) cause
metamorphic changes
Hormones have different effects depending on location in body
Timing of changes regulated by tissue dependent hormone sensitivity
Thyroid receptor is transcriptional repressor until thyroid hormone binds causing it
to become a transcriptional activator
Positive feedback loop is established between thyroid hormone and pituitary gland
allowing incremental increases in hormone concentration
Pituitary
垂体
Metamorphosis
Thyroid
Thyroid Hormones (T3 and
T 4)
Transcriptional
Activation
HIGH
LOW
Number of Receptors
in Affected Tissue
Amount of Hormone
LOW
HIGH
T3
Early Response:
Transcription
Factors
RXR
Binding Site

Late Response:
Transcription initiated
by Transcription
Factors
TH does not determine the developmental
program, but initiates it
• Changing the location of tissue or organ does not alter its
response to TH
• Transplant eye to tail region
– Differentiates & grows into eye in response to TH while tail
regresses
• Transplant tail to trunk
– Tail regresses while limb grows
Tissue Repair
Regeneration,
repair & healing
of injured tissues
Regeneration
Growth of cells and tissues to replace
lost structures
Requires an intact connective tissue
scaffold
Regeneration of vertebrates
There are two types of regeneration:
1.
Epimorphosis or epimorphic regeneration :
This type of regeneration involve the reconstruction of the missing parts
by local proliferation from the blastema, or addition of parts to
remaining piece . For example: regeneration of tail, limbs and lens in
anurans and urodels and other vertebrates.
2. Morpholaxis or morphollactic regeneration:
This type of regeneration involving reorganization of the remaining part of
the body of an animal.For example: Hydra, planaria and other
invertebrates e.g. regeneration of the new individual from body pieces.
Regeneration of Limb
Regeneration begins in 3 phases :
1.
Phase of wound healing or pre -blastema stage :
Blood clotting and migration of epidermal cells from the basal layer of epidermis toward the centre
of the wound. The wound is covered with epithelium which is thicker than the epidermis of the limb .
2. Phase of blastema formation :
Cells accumulate beneath the epithelial covering and formed the blastema. Mesenchymal cells
accumulate beneath the cap . Mesenchymal – blastemal cells differentiate into myoblasts and
muscle cells, early cartilage cells and cartilage. During the dedifferentiate phase Hyaluronate (HA透
明质酸) increases in the distal stump to form blastema . As the blastema forms, the HA will be
decrease. The production of HA and break down of collagen represent the establishment of
migration from stump tissues .
3. Phase of dedifferentiate and morphogenesis :
The blastema begins to restore the part of which the limb was deprived. Specifically, if the fore arm
is removed, the blastema differentiated directly into the muscle, bone, cartilage and skin of the fore
arm.
Tissue
response to
injury. Repair
after injury
can occur by
regeneration,
which
restores
normal
tissue, or by
healing,
which leads
to scar
formation
and fibrosis.
TYPES OF CELLS
• Labile cells
• Stable cells
• Permanent cells
Labile cells
• have a high rate of loss and replacement and
therefore high capacity for regeneration.
• squamous and glandular epithelia
• haemopoeitic cells in bone marrow
Stable cells
• do not normally proliferate but can be
stimulated to do so after damage.
•
•
•
•
•
renal tubular cells,
hepatocytes,
osteoblasts,
endothelial cells,
fibroblasts.
Permanent cells
• Permanent cells : unable to divide after initial
development and therefore cannot regenerate
when some are lost.
• Neurons
• Skeletal & cardiac muscle
Repair Involves
• Regeneration of injured tissue by parechymal
cells of the same type
• Replacement by connective tissue (fibrosis),
resulting in a scar
• In most cases tissue repair involves both of
these two processes.
Repair by Connective Tissue (Fibrosis)
• Fibrosis consists of four components
– formation of new blood vessels (angiogenesis)
– migration and proliferation of fibroblasts
– deposition of ECM
– maturation and reorganization of the fibrous
tissue (remodeling)
Biology of Aging
Some age
gracefully...
Goldie Jean Studlendgehawn
born on November 21, 1945
Animal Models in Aging
 Short lives, experimental results
collected quickly, or over many
generations;
 Maintained easily and inexpensively,
present less complex genetic or
physiological systems than humans.
Caenorhabditis
elegans
Drosophila
melanogaster
Saccharomyces
cerevisiae
Genetically engineered animal models
for exploring the basic mechanisms
involved in the aging
Mus musculus
Theories of Aging:
•
•
•
•
Oxidative Damage
Telomeres
Genetic Alterations with aging
Mitochondrial Aging
Other processes involved:
• Inflammatory processes
• Hormonal changes
• Life style choices
Oxidative stress:
imbalance production/breakdown
• Free radicals are normal products of metabolism
• Predominant cellular free radicals are:
- superoxide (O2 -)
- hydroxyl (OH-)
- nitrogen dioxide (NO2)
superoxide
- hydrogen peroxide (H2O2)
Oxidative stress can lead to:
• Damage to mitochondria, DNA, protein processing and
cellular metabolism
- lipid peroxidation
- protein oxidation
- DNA oxidation
• This ultimately leads to:
- Loss of cellular phenotype
- Necrosis
- or Apoptosis
Endogenous defense mechanisms:
O2
H2O
Mitochondria
P450 oxidases
Catalase
O2-
SOD
H2O2
OH+
H2O
2 GSH
Aging↓
Glutathione
Reductase
Glutathione
Peroxidase
GSSG
H2O
Telomeres and Aging
• Repetitive DNA sequences
At the ends of all human
Chromosomes
From: Aditya Rana in Biotechnology
• In humans there are 46 chromosomes; thus 92
telomeres (one per end)
• Telomere is about 10 to 15 kb in length,
composed of the tandem repeat sequence:
TTAGGG
• Without telomeres, ends of
chromosomes would be
“repaired”, leading to
chromosome fusion and
abnormal function
• Telomeres regulate how
many times a cell can divide.
Telomere sequences
shorten each time DNA
replicates
• Once telomeres shrink to a
certain level, cells can no
longer divide; hence aging
From: National Institutes on
Aging (not protected by
copyright); official domain
Summary of Telomere theory:
Telomere length declines in dividing cells as we age
Telomere length in bp
(human blood cells)
8,000
3,000
1,500
0
35
Age in years
65
Genes that affect Aging:
•
•
•
•
•
Stress resistance genes
Genes targeting inflammation
Genes that slow basic metabolism, like IGF
Overall genetic stability
The problem:
Altered gene expression resulting from quality
control defects allows errors to accumulate as cells
divide leads to cells with diminished function
Many genes shown to influence life span are involved in
DNA damage repair and protection.
Progeria:
• Two forms in humans;
Werner's syndrome (adultonset progeria) and
Hutchinson-Gilford
syndrome (juvenile-onset
progeria).
• Most clinicians believe that
progeria is segmental aging
• Mutation in Werner’s codes
for a DNA helicase (DNA
repair/unwind)
From: www.immortalhumans.com/982/
From:http://www.scripps.edu/~jjperry/research.html
Progeria
Werner’s syndrome:
- chromosome instability syndromes
-Inability to repair DNA
-Increased rate of cancer
-mutated helicase
-inherited as autosomal recessive
Hutchinson-Gilford:
-no helicase abnormality
-The pattern of inheritance is uncertain
-have shorter than normal telomeres
-undergo early cell senescence.
Mitochondrial
Aging
Mitochondrial
DNA is extra
sensitive to
damage, such as
oxidative stress
because it does
not have repair
mechanisms like
normal DNA
Summary of mitochondrial theory:
• Decreased activity of electron transport chain
complex with aging
• Increased release of ROS
• Alterations in mitochondrial apoptosis
pathways (Bax/Bcl-2 etc)
• Lack of repair mechanisms mtDNA
• Slower mitochondrial turnover accumulates
mtDNA mutations
Genomic Alterations with Aging:
Intact telomeric
DNA
Intact nuclear
DNA
Intact mtDNA
Endogenous
oxidative stress
DNA repair
Damaged/shorter
telomeric DNA
Cell cycle arrest
senescence
Damaged nuclear
DNA
Mutation
and cancer
Apoptosis
Cell loss
Aging
Damaged mtDNA
Diminished
energy
production