5. Asymmetric cell division and cell polarity Flashcards

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1
Q

How is “polarity” defined?

A

Asymmetric distribution of molecules, compartments or structures along the axis.

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2
Q

What does it mean for a plant if it has a gnom-mutation?

A

Defects of cell polarity and asymmetric division of the zygote of gnom mutants correlate with defective cell polarity in seedlings. GNOM is (e.g.) required for coordinating polar positioning of positing of Auxin efflux carrier PIN1 in the embryo.

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3
Q

How can you investigate the Auxin distribution in At embryo?

A

Use the Auxin respone-reporter DR5rev::GFP. It is compoted of synthetic auxin-responsive promotor elements driving GFP expression. The Auxin response in the embryo provides an approximation of Auxin distribution.

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4
Q

When is PIN activity needed?

A

Triple PIN mutations show that PIN gen activity is needed during polar axis formation in the embryo similar to GNOM function.

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5
Q

Where is PIN7 localized?

A

Apically early on and switches to basal later on. PIN7 has required for correct cell division orientation contributing to the apical part of the early embryo.; a PIN7 mutant (early embryo) has too much anticlinal division.

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6
Q

How can the PIN1 protein recycling from and to the basal membrane can be reversibly be inhibited?

A

With the vesicle trafficking inhibitor brefeldin A (BFA); gnom in needed for the recycling. With the protein translation inhibitor CHX (cycloheximide) one can see where the protein comes from (PIN goes back)

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7
Q

What does Brefelin A (also) inhibits? With which causes? (mit welchen Folgen)

A

BFA inhibits PIN2 and sterol recycling and causes accumulation if trans-Golgi-derived vesicles in the cell

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8
Q

How can you investigate, where PIN 2 got there for the first time?

A

With the green-to-red photoconversion of PIN2-Dendra reveals polar apical protein secretory delivery in At.
Dendra and EOS: photoswitchable protein; green signal: newly sinthezides; magentha signal: photoconverted
Green fluorescence exited at 488 nm excitation (little red fluorescence at 561 nm excitation)
Briefly locally exite with UV (365 or 405 nm) to photoconverte
Track resultin red fluorescent at 561 nm excitation
PIN2- GFP polarity re-establoshment relies on endocytosis mediated by clathrin, TPLATE-complex, dynamin-related protein (DRP1A) and sterols

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9
Q

When is PIN polarity first established and where?

A

Directly after cell devision via polar secretory targeting and endocytosis; degradation: no transcytosism just vacuolar degredation ; recycle and newly delivered

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10
Q

Protein physphorylation in PIN protein and activity – what do you have in mind?

A

The PINOID protein kinase may direct PIN1 polarity
PINOID, WAG1 and WAG2 mediate apical PIN2 polarity re-establishment after cytokinesis.
PINOID and Protein Phosphatase 2A subunits may antagonistically regulate PIN1 and PIN2 polarity by phosphorylation /dephosphorilation
The PINOID and the D6 Protein Kinase activate the auxin efflux activity conferred by PIN1.

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11
Q

Which 2 players causes an opposite polar PIN protein trafficking?

A

PID phosphorylation and PP2A dephosphorylation

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12
Q

Name three “basic helix-loop-helix (bHLH)” transcription factors regulate different transitions during stomata development

A

SPEECHLESS (SPCH), MUTE and FAMA

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13
Q

The asymmetric distribution of BASL defines daughter cell fate… but how?

A

via the degradation of SPEECHLESS (SPCH) after cell division

External signals may regulate SPCH removal via BASL/YDA /MPK3 /MPK6

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