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
2
Q
1st meiotic devision products
A
- 2 secondary spermatocytes 2N
or - 1 secondary oocyte + 1 polar body 2N
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
4
Q
homologous chromosomes
A
- same type of info but may be different
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
6
Q
2nd meiotic division
A
- chromatids split at centromere: sisters segregate
- completion: ch in each daughter cells are different
7
Q
crossing over and casual segregation
A
- enhance genetic variability
- crossing over in prophase 1
- exchanges are random
- separation in anaphases are random
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
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
10
Q
lysosomes
A
- digesting food and invaders
- recycling cellular components
- cell suicide
- not found in plant cells
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
12
Q
lysosomal storage diseases
A
- more than 40
- fabry disease
- gaucher disease
- hurler syndrome
- lack of enzymes
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
14
Q
cells with lots of peroxisomes
A
- immunity cells
- hepatocytes
15
Q
cells with lots of mitochondria
A
- muscle cells
- spermatozoa
- epithelia
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
