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Complete and Incomplete Metamorphosis. Metamorphosis refers to the way that certain organisms develop, grow, and change form. Metamorphosis actually means.

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Presentation on theme: "Complete and Incomplete Metamorphosis. Metamorphosis refers to the way that certain organisms develop, grow, and change form. Metamorphosis actually means."— Presentation transcript:

1 Complete and Incomplete Metamorphosis

2 Metamorphosis refers to the way that certain organisms develop, grow, and change form. Metamorphosis actually means "change". What is metamorphosis?

3 Franz Kafka 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

4 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.) Two Types of Metamorphosis


6 EGG The female lays eggs.

7 LARVA Larva hatch from the eggs. They do not look like adult insects. They usually have a worm- like 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.

8 ADULT Inside the cocoon, the larvae change into adults. After a period of time, the adult breaks out of the cocoon.

9 Let’s take a closer look at each stage! INCOMPLETE METAMORPHOSIS


11 EGG A female insect lays eggs. These eggs are often covered by an egg case which protects the eggs and holds them together.

12 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.

13 ADULT The insects stop molting when they reach their adult size. By this time, they have also grown wings.

14 Endocrine cells release protein and non-protein hormones Synthesis of hormones is orchestrated by the CNS Hormones effects are tissue dependent 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

15 Hormonal Control of Insect Metamorphosis Brain Temperature, Light, Stress, etc. Prothoracic Gland 前胸腺 Ecdysteroid 蜕皮 激素 Corpus Allatum 咽侧体 Prothoracicotropic 促前 胸腺 hormone (PTTH) Juvenile Hormone (JH) 保 幼激素 Larva Pupa Adult

16 Control of Metamorphosis by Internal and External Factors Temperature (day degrees) Critical size matched (availability of food) Light (photoperiod) Chemicals Amount of moisture ( 湿度 ) Stress: mutagens, predators ( 肉食者 ), etc. Brain Temperature, Light, Stress, etc.

17 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 EcR USP Binding Site Early Response: Transcription Factors Late Response: Transcription initiated by Transcription Factors

18 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

19 Alternative Splicing of Ecdysone Receptor Pre- mRNA Creates Several Forms of the Ec- Receptor Allowing Cell Type Specific Ecdysone Response

20 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) Regulation of JH Levels Amount of Hormone Larva Pupa Adult Juvenile Hormone Ecdysone

21 Metamorphosis in Action: Remember Imaginal Discs? Immature Insect: + JH Adult Insect: - JH

22 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

23 Frogs: Tadpole to Adult

24 Hormonal Control of Frog Metamorphosis Secretions of two hormones, thyroxine (T 4 ) and triiodothyronine (T 3 ) 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

25 Pituitary 垂体 Thyroid Thyroid Hormones (T 3 and T 4 ) Transcriptional Activation Metamorphosis

26 T3T3 TR RXR Binding Site Late Response: Transcription initiated by Transcription Factors Number of Receptors in Affected Tissue Amount of Hormone HIGH LOW HIGH LOW  Early Response: Transcription Factors

27 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


29 Tissue Repair Regeneration, repair & healing of injured tissues

30 Regeneration Growth of cells and tissues to replace lost structures Requires an intact connective tissue scaffold

31 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.

32 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.





37 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.



40 TYPES OF CELLS Labile cells Stable cells Permanent cells

41 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

42 Stable cells do not normally proliferate but can be stimulated to do so after damage. renal tubular cells, hepatocytes, osteoblasts, endothelial cells, fibroblasts.

43 Permanent cells Permanent cells : unable to divide after initial development and therefore cannot regenerate when some are lost. Neurons Skeletal & cardiac muscle

44 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.

45 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)


47 Biology of Aging

48 Goldie Jean Studlendgehawn born on November 21, 1945 Some age gracefully...




52 Animal Models in Aging Saccharomyces cerevisiae Caenorhabditis elegans Drosophila melanogaster Mus musculus  Short lives, experimental results collected quickly, or over many generations;  Maintained easily and inexpensively, present less complex genetic or physiological systems than humans.  Genetically engineered animal models for exploring the basic mechanisms involved in the aging

53 Theories of Aging: Oxidative Damage Telomeres Genetic Alterations with aging Mitochondrial Aging Other processes involved: Inflammatory processes Hormonal changes Life style choices

54 Oxidative stress: imbalance production/breakdown Free radicals are normal products of metabolism Predominant cellular free radicals are: - superoxide (O 2 - ) - hydroxyl (OH - ) - nitrogen dioxide (NO 2 ) - hydrogen peroxide (H 2 O 2 ) superoxide

55 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

56 Endogenous defense mechanisms: O2-O2- H2OH2OOH + H2O2H2O2 Mitochondria P450 oxidases O2O2 SOD GSSG 2 GSH Catalase GlutathionePeroxidase H2OH2O GlutathioneReductase H2OH2O Aging ↓

57 Telomeres and Aging Repetitive DNA sequences At the ends of all human Chromosomes 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 From: Aditya Rana in Biotechnology

58 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

59 Summary of Telomere theory: Telomere length in bp (human blood cells) Telomere length declines in dividing cells as we age 8,000 1,500 3,000 0 35 65 Age in years

60 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

61 Many genes shown to influence life span are involved in DNA damage repair and protection.

62 Progeria: Two forms in humans; Werner's syndrome (adult- onset 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: From:

63 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.

64 Mitochondrial Aging Mitochondrial DNA is extra sensitive to damage, such as oxidative stress because it does not have repair mechanisms like normal DNA

65 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

66 Genomic Alterations with Aging: Intact telomeric DNA Damaged/shorter telomeric DNA Intact nuclear DNA Damaged nuclear DNA Intact mtDNA Damaged mtDNA Endogenous oxidative stress Aging Cell cycle arrest senescence Apoptosis Cell loss Mutation and cancer Diminished energy production DNA repair

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