Lecture 9 Flashcards
How does secondary growth in roots occur?
When residual procambium in the xylem and phloem become meristematic (reactive and begin dividing) the pericycle opposite the xylem also begins dividing
What happens to the two types of pericycle during secondary growth in roots? (Aka. What do they form?)
The meristematic pericycle/residual procambium form a continuous ring around the xylem to form the root vascular cambium while the remaining pericycle forms the first cork cambium
Strategies for controlling plant development (3)
Regulate cell division (rate/direction/polarity of division)
Cell expansion (direction/length/uniformity of expansion)
Cell differentiation and specialization (positive/negative regulation, cell specialization during maturation)
Cell cycling occurs in specific plant zones. Explain where they are found (location/timing) in monocots and eudicots.
Monocots: cell division zones are localized (RAM at bottom tip, SAM at dome)
Eudicots: cell division zones move from taking up the entire cell when introduced to negligent when mature (cycle through proliferation -> expansion -> maturation)
Vascular differentiation in eudicots fills in the lead with veins by what mechanism?
Form a central vein from base to top then fill in spaces with minor veins from tip to base
When is photosynthetic physiology established?
At the end of cell division, shortly after cells have all matured
(Initially decline due to nutrient deprivation in competition with younger leaves)
Leaf senescence pathway (3)
Age/hormones/stresses -> signal transduction -> transcription factors
Transcription factors associated with inhibiting/promoting lead senescence (2)
SDG: inhibit senescence by down-regulating senescence genes (photosynthetic genes)
SAG: a senescence-associated gene that promotes senescence (proteases, nucleases, lipases)
SAG’s promote what (2)
Degradation Nutrient recycling (retrieving nutrients from the old leaf and transmitting them to young leaves (cannibalizes old))
Layers of leaf that form during senescence (2)
Separation layer (where cell wall breaks down) Protective layer (protects leaf from bacterial penetration)
The cell cycle (2 sections, 3 phases, 2 checkpoints)
2 sections: interphase, mitosis and cytokinesis
3 phases (in interphase):
- G1 (synthesis of cytoplasm + components)
- S (DNA synthesis)
- G2 (prep for mitosis, nuclear migration, cytoskeletal formation)
2 checkpoints: G1 -> S, G2-> M
Purpose of checkpoints
To ensure the previous phase was carried out accurately
What are CDKs?
CDKs are regulated by (3)? Cyclin is regulated by (2)? When activated both imitate which cell cycle phase?
CDKs are protein kinases that phosphorylate proteins using ATP to control their function/the downstream pathway
CDKs regulated by: cyclin, phosphorylationC dephosphorylation
Cyclin regulated by: synthesis, degradation
Activated-CDKs initiate mitotic division
Activated-cyclin initiates S phase
What is a cytoskeleton and what does it compose of (3)?
A dynamic network of protein filaments within the cytosol
Composed of: microtubules, actin filaments, intermediary filaments
Cytoskeleton function (6)
Moves/positions organelles
Positions protein complexes on organelles/plasmalemma
Moves vesicles to plasma membrane (during exocytosis)
Drives cell division
Orientation of cell expansion/differentiation
Positions wall divers (for a normal cell)
Cytoskeleton during mitosis/cytokinesis
Mitosis: cortical microtubules -> preprophase band -> mitotic spindle -> phragmoplast
Cytokinesis: cell plate forms between microtubules -> -> microtubules realign to original position
Cytoskeleton and mitotic spindle initiation process of pulling apart
Spindle fibres attach to protein complexes to make kinetochores that bind to the sides of the chromatid OR send a signal to inhibit anaphase
When all kinetochores are attached an inhibitory signal is activated, APC (prevents metaphase -> anaphase) is activated and ubiquitin is coupled to cyclin
Cyclin degrades and motors pulling chromatids are activated
Actin/microtubule placement essential for (5)
Correct cell plate positioning Control of directional cell expansion Single cell morphogenesis Cell differentiation Cell-to-cell communication
Stomatal development pathway (4)
Postprotodermal cell -> meristemoid mother cell -> meristemoid -> guard cell
What is the point of inhibitory proteins in stomatal development?
Induce negative regulation that establishes the placement of guard cells so that they are not too close to one another (form a basipetal pattern)
Role of CDKs in stomatal development
Regulation of CDKs is crucial
If reduce activity of B1-type CDKs
- fail to undergo the final guard cell division (abnormal cells blocked in G2 phase)
- have a decrease in stomatal density (meristemoid division is blocked; satellite meristemoid formation is inhibited) t
Mechanisms of cell expansion (3)
Cell wall loosening
Water uptake
Generation of a new wall
Patterns of expansion (4)
Non-polar growth
Polar growth
Localized (tip) growth
Regulation of growth direction
Role of microtubules and actin filaments in directional growth
Microtubules: align perpendicular to expansion and control placement of cellulose during expansion
Actin filaments: don’t have a specific alignment; move Golgi-produced vesicles to cell periphery
