Lecture 9 Flashcards

1
Q

How does secondary growth in roots occur?

A

When residual procambium in the xylem and phloem become meristematic (reactive and begin dividing) the pericycle opposite the xylem also begins dividing

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2
Q

What happens to the two types of pericycle during secondary growth in roots? (Aka. What do they form?)

A

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

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3
Q

Strategies for controlling plant development (3)

A

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)

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4
Q

Cell cycling occurs in specific plant zones. Explain where they are found (location/timing) in monocots and eudicots.

A

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)

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5
Q

Vascular differentiation in eudicots fills in the lead with veins by what mechanism?

A

Form a central vein from base to top then fill in spaces with minor veins from tip to base

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6
Q

When is photosynthetic physiology established?

A

At the end of cell division, shortly after cells have all matured

(Initially decline due to nutrient deprivation in competition with younger leaves)

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7
Q

Leaf senescence pathway (3)

A

Age/hormones/stresses -> signal transduction -> transcription factors

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8
Q

Transcription factors associated with inhibiting/promoting lead senescence (2)

A

SDG: inhibit senescence by down-regulating senescence genes (photosynthetic genes)

SAG: a senescence-associated gene that promotes senescence (proteases, nucleases, lipases)

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9
Q

SAG’s promote what (2)

A
Degradation
Nutrient recycling (retrieving nutrients from the old leaf and transmitting them to young leaves (cannibalizes old))
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10
Q

Layers of leaf that form during senescence (2)

A
Separation layer (where cell wall breaks down)
Protective layer (protects leaf from bacterial penetration)
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11
Q

The cell cycle (2 sections, 3 phases, 2 checkpoints)

A

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

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12
Q

Purpose of checkpoints

A

To ensure the previous phase was carried out accurately

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13
Q

What are CDKs?

CDKs are regulated by (3)? Cyclin is regulated by (2)? When activated both imitate which cell cycle phase?

A

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

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14
Q

What is a cytoskeleton and what does it compose of (3)?

A

A dynamic network of protein filaments within the cytosol

Composed of: microtubules, actin filaments, intermediary filaments

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15
Q

Cytoskeleton function (6)

A

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)

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16
Q

Cytoskeleton during mitosis/cytokinesis

A

Mitosis: cortical microtubules -> preprophase band -> mitotic spindle -> phragmoplast

Cytokinesis: cell plate forms between microtubules -> -> microtubules realign to original position

17
Q

Cytoskeleton and mitotic spindle initiation process of pulling apart

A

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

18
Q

Actin/microtubule placement essential for (5)

A
Correct cell plate positioning
Control of directional cell expansion
Single cell morphogenesis 
Cell differentiation 
Cell-to-cell communication
19
Q

Stomatal development pathway (4)

A

Postprotodermal cell -> meristemoid mother cell -> meristemoid -> guard cell

20
Q

What is the point of inhibitory proteins in stomatal development?

A

Induce negative regulation that establishes the placement of guard cells so that they are not too close to one another (form a basipetal pattern)

21
Q

Role of CDKs in stomatal development

A

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
22
Q

Mechanisms of cell expansion (3)

A

Cell wall loosening
Water uptake
Generation of a new wall

23
Q

Patterns of expansion (4)

A

Non-polar growth
Polar growth
Localized (tip) growth
Regulation of growth direction

24
Q

Role of microtubules and actin filaments in directional growth

A

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

25
Q

What happens to an expanding cell treated with tubulin inhibitors?

A

Leads to non-directional cell expansion making blobs

26
Q

What controls the orientation of cellulose microfibrils?

A

The positioning of microtubules in the outer cytoplasm

27
Q

Patterns of expansion (3)

A

Non-polar growth (isotropic: even in all directions)

Polar growth (ansiotropic: uneven growth in one direction)

Localized (tip) growth (transverse microfibrils/cortical fibres have polar growth, randomly oriented microfibrils) (make Root hair)

28
Q

When does trichome elongation occur? Stopped?

Arrangement of microtubules throughout trichome elongation (2)

A

Elongation occurs during interphase
Cells are stopped in the G1 phase

Arrangement:
- cortical microtubules align perpendicularly
> cellulose microfibrils follow accordingly
> elongation and secondary cell wall synthesis occur
- microtubules align in a steeply pitched manner

29
Q

What are cotton fibres made of? Mechanisms of cotton boll formation (2)

A

Made of elongated trichomes from the seed coat

Mechanisms:
Cell wall loosening (increase expansin mRNA levels)
Uptake of water following surge of osmotically active solutes (provide turgor for expansion)

30
Q

Mechanism of water uptake induced by osmotica (7)

What is this process called?

A

Trichomes become symplastically isolated
Callose is deposited into the plasmalemma to intensify the osmotic potential and pressure potential difference
Osmotica accumulates in symplast
Water potential decreases
Water flows in
Generates turgor pressure
Cell expands

Process is called: Plasmodesmatal Gating

31
Q

Turgor driven processes in plants (7)

A

Stomatal opening (PD occluded at maturity)

Cell expansion during growth (temporary PD occlusion)

Leaf movement (uncertain)

Root pressure (uncertain)

Phloem transport (PD occlusion in apoplast loaders/PD size limited in symplast loaders)

Tropisms (PD occlusion by callose localize expansion)