Lecture 6 - Molecular Genetic Basis of Development – Cell Commitment and Differentiation Flashcards
how are trichome formed?
Trichome mutants are altered in either number, distribution or morphology of trichomes
At least 25 genes can mutate to alter trichome development
what is cell commitment?
Commitment of cells to follow particular developmental fates is a key aspect of morphogenesis
As an example, see how cell commitment is controlled in the plant epidermis
how is the regulation of development in the epidermis?
The epidermis is the outer single cell layer covering the organs of the plant
Leaf epidermal cells:Pavement cells, Stomatal guard cells, Trichomes
Even spatial distribution
what are root epidermal cells?
Hair cells
Non-hair cells
what are seed epidermal cells?
No differentiation of different cell types;
synthesises brown pigment
What specifies particular leaf and root epidermal cells to follow particular developmental fates?
To identify genes controlling epidermal cell fate use a forward genetic approach, i.e. isolate mutants and identify the corresponding wild-type genes
what are 2 mutants that have essentially no trichomes?
glabra 1 (gl1)
transparent testa glabra 1 (ttg1)
Therefore GL1 and TTG1 genes in the wild-type are required for commitment of leaf epidermal cells to differentiate into a trichome, i.e. specify epidermal cell fate
GL1 is a transcription factor
TTG1 protein binds to GL1 and is required
for GL1 action
what glabra3 mutants?
glabra3 (gl3) mutants have fewer trichomes than WT. So GL3 positively regulates trichome cell fate.
GL3 is a transcription factor that forms a protein complex with TTG1 and GL1.
The GL1, GL3, TTG1 complex is a positive regulator that switches on genes in the trichome differentiation pathway.
Target genes include other transcription factors, which regulate sets of genes; cell differentiation often involves sequential activation of transcription factors.
Why are trichomes evenly distributed across the wild-type epidermis?
It appears that cells that commit to form trichomes also produce signals that repress trichome formation in adjacent cells, i.e. negative regulators
what are stomatal cell guards?
Stomatal guard cells are also produced from leaf epidermal cells and are evenly spaced over the epidermis
what are the 3 transcription factors?
SPEECHLESS, MUTE and FAMA - control the steps in stomatal formation
SPEECHLESS is required to initiate stomatal morphogenesis
MUTE and FAMA control later steps in stomatal development
how is root hair formations?
-In contrast to leaf hairs, root hairs
arise in a position-dependent pattern
-Hair cells arise at the junctions between adjacent cortical cells
-The root has files of hair and non-hair cells
what is Over-expression of GL3?
The GL1, GL3, TTG1 complex is a positive regulator, i.e. promotes trichome production
Transgenic plants can be made which over-express the complex. This results in over-production of trichomes
how does TTG1 act in epidermal cells throughout the plant?
In the seed epidermis TTG1 associates with transcription factors to control synthesis of the brown pigments called condensed tannins.
The seed epidermis is called the testa, hence the name of the ttg1 mutant -transparent testa
The ttg1 mutant also has ectopic root hair production
Therefore TTG1, like WER specifies non-hair cell fate
A screen for mutants with clusters of trichomes identified triptychon and caprice…
These mutants lack the repressive signal that prevents trichome clustering
TRY and CPC are transcription factors that cause repression of trichome production – negative regulators
Transgenic plants over-expressing TRY and CPC lack trichomes
how do distorted mutants make trichomes?
E.g. distorted (dis) mutants can make trichomes but have abnormal trichome morphology
A double mutant of gl1 and dis1 has no trichomes. This shows that gl1 is epistatic to dis1 and that GL1 functions before DIS1 in the trichome differentiation pathway
what is the tmm mutant?
The two many mouths (tmm) mutant has clusters of stomata
Therefore TMM in wild-type controls the spatial distribution of stomatal production
Mutants altered in stomatal development are not altered in trichome formation and trichome mutants are not altered in stomatal development, so the fates of leaf trichome and stomatal cells are controlled independently
what is the wer mutant
The werewolf (wer) mutant is hairy and produces hairs from non-hair cells. This is called ectopic root hair production.
Therefore, in wild-type, WER acts to repress hair formation in non-hair cells i.e. specifies
non-hair cell fate.
The WER gene encodes a transcription factor and is expressed in non-hair cells to switch on a gene that produces a repressor of hair production.
how does TTG1 function with WER?
TTG1 functions with WER to repress hair production and specify non-hair cell fate
Non-hair cells produce a signal that represses the action of WER/TTG1 in adjacent cells, causing hair production
In addition, a signal from the underlying cortical cells inhibits WER expression in hair cells: positional information
