Growth Development of Organisms.docx

[Growth Development of Organisms ] Human embryonic development: 'egg' germinal period = 0-3^rd^ weeks Embryo = 3-8^th^ weeks Foetus = 8-38^th^ weeks Trimester 1 = 0-12^th^ week Trimester 2 = 12-26^th^ week Trimester 3 = 26^th^-fullterm [Critical Period ] - Development stage where embryo i...

[Growth Development of Organisms ] Human embryonic development: 'egg' germinal period = 0-3^rd^ weeks Embryo = 3-8^th^ weeks Foetus = 8-38^th^ weeks Trimester 1 = 0-12^th^ week Trimester 2 = 12-26^th^ week Trimester 3 = 26^th^-fullterm [Critical Period ] - Development stage where embryo is most suspectable to toxic agents (teratogen) - Usually responds to stage of active differentiation and morphogenesis - Varies depending on organs Possible teratogen: Medication -- Thalidomide (sedative) Alcohol, tobacco, caffeine Environmental factors Viral infection After implantation occurs at blastocyst stage (implantation = day 8-9) Following gastrulation 3 germ layers are formed: Derivatives of these 3 germ layers (what they form): Ectoderm - Surface ectoderm (mainly surface of the skin) - Nervous system - Neural crest cell derivatives e.g. melanocytes, some skull, bones adrenal medulla Mesoderm: - Dermis (inner layer of skin) - Muscles - Skeleton - Urogenital organs (except urinary bladder) - Blood, vasculature, spleen Endoderm: - The digestive system (Gut, liver, pancreas) - Respiratory system - Urinary bladder - Thyroid, parathyroid [Growth of foetus ] Day 1 = Morphogenesis and Differentiation Day 10-20 = Rapid Growth Day 20-30 = Protein Accumulation Day 30-40 = Fat Accumulation [Hormones involved in Growth:] - GH (Growth Hormone) - IGF-1 (Insulin like Growth Factor 1) - Gonadotropin-releasing hormone (GnRH) - Gonadal steroids (Androgen, Oestrogen, Progestogen) - Others e.g. Thyroid hormones, Calcitonin, Parathyroid hormones, Corticosteroids [Effects of GH] Stimulates glycogenolysis in liver raises plasma glucose levels more glucose available for glycolysis Represses glucose uptake by muscle + adipose tissue Stimulates lipolysis Stimulates amino acid uptake protein synthesis Causes production of IGF-1 in liver [Gonadotropin-releasing Hormone (GnRH)] Increased activity of hypothalamic GnRH-secreting neurons Increase of Follicle stimulating hormone (FSH) and Luteinising hormone (LH) Puberty, Females = ovarian follicles mature, Males = testosterone secretion and spermatogenesis [Cell Renewal ] Renew by Stem cells: - Skin epidermis - Blood cells - Intestinal epithelium - Olfactory neurons (rodents) Renew without Stem cells: - Insulin producing B-cells - Hepatocytes in liver Cells which do not renew: - Auditory cells - Photoreceptor cells [Stem cell categories:] Embryonic stem cells - pluripotent Adult stem cells. -- multipotent Induced pluripotent (iPS) stem cells -- pluripotent Fetal stem cells -- multipotent [Adult stem cells:] Hematopoietic stem cells Dermal papilla cells (hair follicle stem cells) Intestinal stem cells -- can differentiate into: Absorptive cells, Goblet cells, Enteroendocrine cell and Paneth cell Mesenchymal stem cells Limbal stem cells -- margin of cornea (limbus) Satellite cells - in muscles Neural stem cells -- in subventricular zone [Ageing] Quiescence -- cell cycle stuck in G0 due to lack of nutrition or no stimulus for cell division Senescence - from G0 to cell death eventually, through cells are metabolically active Hall marks of ageing: Genomic instability, Telomere attrition, Epigenetic alterations, loss of proteostasis, Deregulated nutrient-sensing, Mitochondrial dysfunction, Cellular senescence, Stem cell exhaustion. Accumulation of mutations and epigenetic factors in the genome. Typical 70yr old has 2000 gene 'scars' (traces of gene mutations) across genome. Mitochondrial mutations occur 1000x more due to toxic ROS (reactive oxygen species) \*They can fuse and divide thus exchanging DNA [Senescence ] Most cells only divide limited number of times due to chromosomes becoming shorter at the ends (telomere) Therefore, short telomere detected as damaged DNA cell cycle is stopped at p53 [Telomere] - Repetitive DNA sequences at end of chromosomes in human - Forms loop so it is not recognised as broken - Requires 'Telomerase' for replication - Stem cells express higher levels of telomere allowing for replication without loss of it - Whilst most other cells express low levels of telomere - Every cell division 100-200 nucleotides are removed from telomere - Telomere shortening is a mechanism which allows cells to 'count' cell divisions to get rid of old cells and safeguard against uncontrolled replication. \*Telomerase is a reverse transcriptase with bound RNA template - Telomere loss = DNA damage = p53 increase = either Cancer, if dysfunctional p53, or Ageing, if p53 is intact. - P53 -- apoptosis, DNA repair, anti-proliferate - Many cancer cells regained ability to express telomerase so able to proliferate regardless of damaged DNA. - iPS cells (from somatic cells) regain ability to express telmorase.