Epidermal cell fate determination in arabidopsis patterns defined by a steroid-inducible regulator

Stinging trichomes vary in their morphology and distribution between species, however similar effects on large herbivores implies they serve similar functions. In areas susceptible to herbivory, higher densities of stinging trichomes were observed. In Urtica , the stinging trichomes induce a painful sensation lasting for hours upon human contact. This sensation has been attributed as a defense mechanism against large animals and small invertebrates, and plays a role in defense supplementation via secretion of metabolites. Studies suggest that this sensation involves a rapid release of toxin (such as histamine) upon contact and penetration via the globular tips of said trichomes. [14]

Many of the actions of cyclic AMP are carried out by protein kinase A (PKA), which phosphorylates specific sites on downstream effector processes ( Module 2: Figure cyclic AMP signalling ). PKA is composed of two regulatory (R) subunits and two catalytic (C) subunits. The way in which cyclic AMP activates PKA is to bind to the R subunits, which then enables the C subunits to phosphorylate a wide range of different substrates [ Module 2: Figure protein kinase A (PKA) ]. Of the two types of PKA, protein kinase A (PKA) I is found mainly free in the cytoplasm and has a high affinity for cyclic AMP, whereas protein kinase A (PKA) II has a much more precise location by being coupled to the A-kinase-anchoring proteins (AKAPs) . The AKAPs are examples of the scaffolding proteins that function in the spatial organization of signalling pathways by bringing PKA into contact with its many substrates. The scaffolding function of the AKAPs is carried out by various domains such as the conserved PKA-anchoring domain [yellow region in Module 2: Figure protein kinase A (PKA) ], which is a hydrophobic surface that binds to an extended hydrophobic surface on the N-terminal dimerization region of the R subunits. At the other end of the molecule, there are unique targeting domains (blue) that determine the way AKAPs identify and bind specific cellular targets in discrete regions of the cell.

FIGURE 84-3 Schematic diagram of the T-cell interactions with an antigen-presenting cell. The thick gray lines depict the plasma membranes of the interacting cells. The molecules of the antigen-presenting cell, namely LFA-1, ICAM-1 or ICAM-3, LFA-3, MHC class II, and CD80 or CD86, are displayed on top, while the T-cell antigens, ICAM-2, LFA-1, CD2, CD4, the T-cell receptor complex (TCR complex), and CD28, are shown on the bottom of the diagram. Thin lines connecting the stick figures indicate disulfide bridges. The TCR complex consists of the ab heterodimer that is noncovalently coupled with the d, e, g, and z chains of CD3, as indicated. This complex can recognize peptide antigen (designated by the diamond labeled P) that is cradled by the a and b chains of the MHC class II molecule of the antigen-presenting cell. The avidity of this interaction is enhanced by CD4 on the T-cell surface that interacts with nonpolymorphic determinants on the MHC class II molecule. The interaction steps between the T cell and the antigen-presenting cell are listed at the bottom of the figure. T-cell molecules ICAM-2 (CD102), LFA-1 (CD11a/CD18), and CD2 bind to LFA-1, ICAM-1 (CD54) or ICAM-3 (CD50), or LFA-3 (CD58) respectively that are present on the surface of the antigen-presenting cell. These molecules provide for better adhesion between the T cell and the antigen-presenting cell (adhesion), allowing for time for the TCR receptor complex to find the MHC molecule bearing a specific peptide antigen (antigen recognition). Should the antigen-presenting cell express CD80 or CD86, then simultaneous ligation of CD28 will occur (costimulation), leading to activation of the reactive T cell.

The epidermis is sustained by a multipotent stem cell population that gives rise to cells of different fates including those forming hair follicles, interfollicular epidermis and associated glands such as sebaceous glands. The most intriguing evidence comes from using a variety of mouse models with which studies have found the WNT pathway to be involved in regulating stem cell fate decisions. These mouse models have been used to analyze different members of the WNT pathway in the epidermis and altogether suggest that different levels of β-catenin correlate with the adoption of different epidermal stem cell fates. Recent data specifically analyzing c-Myc, a downstream target of the WNT pathway, has found that c-Myc can divert epidermal stem cells to a sebaceous gland fate at the expense of hair follicles. Also, newly emerging data using gene expression profiling techniques have uncovered a more direct role of c-Myc in stem cell fate determination.

Epidermal cell fate determination in arabidopsis patterns defined by a steroid-inducible regulator

epidermal cell fate determination in arabidopsis patterns defined by a steroid-inducible regulator

The epidermis is sustained by a multipotent stem cell population that gives rise to cells of different fates including those forming hair follicles, interfollicular epidermis and associated glands such as sebaceous glands. The most intriguing evidence comes from using a variety of mouse models with which studies have found the WNT pathway to be involved in regulating stem cell fate decisions. These mouse models have been used to analyze different members of the WNT pathway in the epidermis and altogether suggest that different levels of β-catenin correlate with the adoption of different epidermal stem cell fates. Recent data specifically analyzing c-Myc, a downstream target of the WNT pathway, has found that c-Myc can divert epidermal stem cells to a sebaceous gland fate at the expense of hair follicles. Also, newly emerging data using gene expression profiling techniques have uncovered a more direct role of c-Myc in stem cell fate determination.

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