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cytology > meiosis, organelles and cell death > Flashcards

meiosis, organelles and cell death Flashcards

1
Q

sexual reproduction

A
  • requires specialised cells: gametes
  • somatic cells: 44 autosomes and 2 sex ch: diploid: 2n in most cycle and 4n in S and anaphase
  • mature germ cells (gametes): 23 single chromosomes: haploid: 1N
  • fusion of m and f gametes restores non-germ diploid cell
  • requires meiosis to produce haploid cells
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2
Q

1st meiotic devision products

A
  • 2 secondary spermatocytes 2N
    or
  • 1 secondary oocyte + 1 polar body 2N
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3
Q

2nd meiotic division products

A
  • 4 round spermatids 1N
    or
  • 1 oocyte and 3 polar bodies 1N
  • m and f gametogenesis result in different number of gametes
  • primary oocyte produces one mature gamete
  • primary spermatocyte produces four spermatids all developing into spermatozoa
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4
Q

homologous chromosomes

A
  • same type of info but may be different
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5
Q

1st meiotic division

A
  • homologous chromosomes pair (4 chromatids)
  • they interchange chromatid fragments in crossing over (not chiasma)
  • pull apart in anaphase: hmc segregate
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6
Q

2nd meiotic division

A
  • chromatids split at centromere: sisters segregate
  • completion: ch in each daughter cells are different
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7
Q

crossing over and casual segregation

A
  • enhance genetic variability
  • crossing over in prophase 1
  • exchanges are random
  • separation in anaphases are random
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8
Q

primordial germ cells

A
  • PCG, gonocytes
  • both type of germ cells derive from PCGs
  • undergo a few mitotic divisions after they are invested by the somatic support cells which then differentiate into Sertoli cells
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9
Q

gametogenesis

A
  • different time for m and f
    -PCG enter meiosis in the foetal gonad (3-5m)
  • differentiate into spermatogonia
  • male meiosis inhibitor produced by sertoli cells in male gonad: spermatogonia do not proceed into spermatocytes during this phase: do in puberty under testosterone and proceeds thru adult life
  • oogonia are no longer present after 5 month: oocytes present
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10
Q

lysosomes

A
  • digesting food and invaders
  • recycling cellular components
  • cell suicide
  • not found in plant cells
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11
Q

autophagy

A
  • intracellular degradation system that delivers cytoplasmic constituents to the lysosome
  • when cell is deprived
  • reuses junk
  • physiological and pathophysiological roles
    1. sequestration:formation of phagosome
    2. transport to lysosomes
    3. degradation
    4. utilisation of degradation of products
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12
Q

lysosomal storage diseases

A
  • more than 40
  • fabry disease
  • gaucher disease
  • hurler syndrome
  • lack of enzymes
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13
Q

peroxisomes

A
  • single bound membrane organelles
  • contain catalases (redox enymes)
  • catalyse decomposition of hydrogen peroxide into water and oxygen
  • catabolism of long chain fatty acids, bile and intermediates (in liver)
  • beta-oxidation via peroxisomal beta-oxidation system
  • fatty acid oxidation: energy production
  • detoxification of the body
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14
Q

cells with lots of peroxisomes

A
  • immunity cells
  • hepatocytes
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15
Q

cells with lots of mitochondria

A
  • muscle cells
  • spermatozoa
  • epithelia
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16
Q

mitochondria

A
  • all cells except blood cells and terminally keratinocytes
  • number, shape are often characteristic for cell types
  • variety of shapes: spheres, rods, elongated filaments, coiled structures
  • 1000-2000 per cell (30 000 ovocytes)
  • lamellar: Kreb’s cycle: respiration
  • tubular cristae: lipid metabolism
  • ATP synthase complex and electron transport chain in inner membrane generate gradient to produce ATP
  • Ca2+ storage and release
  • apoptosis control
  • localisation meets the need for local ATP production: sperm tail, striated duct of salivary gland, skeletal myofiber, along microtubules
17
Q

mitochondria input and output

A
  • krebs: 6 NADH, 2 FADH= 24 ATP
  • glycolysis: 2NADH + 2 ATP = 8 ATP
18
Q

mitochondrion origin

A
  • evolutionary hypothesis: gradual evolution from reticulum thru functional cloning of existing one
  • endosymbiotic hypothesis
19
Q

microscopy techniques to visualize mitochondria

A
  • fibroblast: phase contrast
  • Normarsky: differential interference contrast (DIC)
  • hepatocyte: hematoxylin
  • epithelial cell: mitotracker
20
Q

intercellular mitochondrial transfer

A
  • TNTs: tunneling nanotubes or microvesicles
  • donator and recipientor
  • from PC12 cells to PC12 cells
  • from Astrocytes to neurons
  • from bone-marrow derived stromal cell to pulmonary alveoli
  • from mesenchymal stem cells to somatic cells
21
Q

mitochondria diseases

A
  • class of diseases causes muscle weakness and neurological disorders due to mito malfunction
  • worn out mito may be important for aging
  • primarily affects children but adult onset becoming more common
  • brain, heart, liver, skeletal muscles, kidney, endocrine, respiratory
22
Q

pompe disease: glycogenosis

A
  • neuromuscular disorder with autosomal recessive transmission
  • lysosomal acid a-glucosesidase (GAA) due to GAA gene mutation
  • accumulation of glycogen in lysosomes
  • failure to dispose of glycogen in muscle reserves: accumulation
  • The impairment of the autophagic‐lysosomal pathway in Pompe disease results into accumulation of dysfunctional mitochondria and defective clearance of reactive oxygen species (ROS), thus leading to increased oxidative stress.
23
Q

tissue homeostasis: balance

A
  • more cell death: neurodegeneration, immunodeficiency, infertility
  • more new cells: cancer, autoimmunity
24
Q

two types of cell death

A
  • apoptosis: programmed cell death
  • necrosis: unprogrammed cell death, injury
  • autophagic death
25
Q

apoptosis

A
  • active, genetically determined process
  • mitochondria and ionic pumps keep working, providing energy for the process
  • junctions break, chromatin condenses near nuclear periphery
  • nucleus, cells are fragmented into membrane bound- enclosed apoptotic bodies
  • bodies phagocytosed by neighbouring cells and roving macrophages
26
Q

uses of apoptosis

A
  • embryonic morphogenesis
  • removal of dangerous cells (killing by immune effector cells)
  • regulation of cell number: : of viability by hormones and growth factors
27
Q

apoptosis early events at ultracellular level

A
  • cell shrinkage
  • budding
  • cytoplasm condensation
  • nuclear fragmentation
  • chromatin condensation beneath the nuclear membrane (picnosis)
  • fragmentation of fibrillar nucleolus (karyorhexis)
28
Q

necrosis

A
  • cell death mediated by signal transduction from receptor-interaction serine/threonine kinase (RIP)1 to RIP3
  • trauma
  • cells and organelles swell
  • chromatin condenses
  • membrane compromised: fluid rushes in
  • dissolution of cellular structures
  • cell lysis
  • invasion of phagocytic cells
  • inflammation
29
Q

necrosis: early events

A

at ultrastructural level
- cell swelling
- mitochondria swelling: loss of cristae
- ER swelling
- lysosome rupture
- organelle disruption

30
Q

necrosis: morphological hallmarks

A
  • cytoplasm: eosinofilic
  • nucleus: fragmentation: karyorhexis
  • whole cell: cell detachment, swelling and leakage, blebs, fragmentation
31
Q

signalling pathways for promoting necroptosis

A
  • cytokines such as TNF and Fas ligand bind to their receptors
  • causing their trimerization and recruitment of adaptor proteins
  • procaspase-8, RIP1 and other proteins activating caspase-8
  • c-8 proteolyzes RIP1 and other substrates to promotre apoptosis
  • RIP1: receptor-interacting serine/threonine kinase
  • ## MLKL: pseudokinase mixed lineage kinase domain-like
  • if c-8 not activated: RIP1 is activated by phosphorylation recruiting RIP3
  • RIP1 phosphorylated RIP3 causing recruitment of MKLK which is then phosphorylated by RIP3
  • ## leads to oligomerization of MKLK: binds to phosphoinositides in membrane to form a pore for Na+ and water to come in causing swelling
  • can also result from activation of toll-like receptors (TLR) like TLR3 and 4
  • RIP3 activated through the binding of an adapter protein to the TLR
  • RIP1 independent mechanism
  • RIP3 activates MKLK which then oligomerizes and forms pores leading to membrane rupture
32
Q

signalling pathways promoting pyroptosis

A

inflammasome
- pyroptosis eliminated microbial pathogens within and outside cells

33
Q

necrosis and apoptosis compared

A

A:
- gene driven
- chromatine condensation, nucleus, fragmentation, cell shrinkage
- phagocytisus of remaining apoptotic bodies by neighbours
N:
- stochastic, triggered by external factors
- membrane disruption, cell swelling
- cell explosion and cell contect dispersion (inflammation)

33
Q

signaling pathways promoting ferroptosis

A
  • triggered by lipid peroxidation
  • GPX4
  • also necessarry is the disruption in iron hoeostasis
  • lipids containing unsat fatty acids are directly oxidised by molecular oxygen

cytology (7 decks)

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