Usage of therapeutic concept for pupils with physical and combined disability

The aim of this Master Thesis is to make a list of therapeutic concepts that are used for physically and multiple disabled pupils in the Grammar schools for the multiple disabled pupils. We will mainly focus on which therapies are offered by these schools and how many pupils use them and make benefit from them

Epithelial rotation is preceded by planar symmetry breaking of actomyosin and protects epithelial tissue from cell deformations

<div><p>Symmetry breaking is involved in many developmental processes that form bodies and organs. One of them is the epithelial rotation of developing tubular and acinar organs. However, how epithelial cells move, how they break symmetry to define their common direction, and what function rotational epithelial motions have remains elusive. Here, we identify a dynamic actomyosin network that breaks symmetry at the basal surface of the <i>Drosophila</i> follicle epithelium of acinar-like primitive organs, called egg chambers, and may represent a candidate force-generation mechanism that underlies the unidirectional motion of this epithelial tissue. We provide evidence that the atypical cadherin Fat2, a key planar cell polarity regulator in <i>Drosophila</i> oogenesis, directs and orchestrates transmission of the intracellular actomyosin asymmetry cue onto a tissue plane in order to break planar actomyosin symmetry, facilitate epithelial rotation in the opposite direction, and direct the elongation of follicle cells. In contrast, loss of this rotational motion results in anisotropic non-muscle Myosin II pulses that are disorganized in plane and causes cell deformations in the epithelial tissue of <i>Drosophila</i> eggs. Our work demonstrates that atypical cadherins play an important role in the control of symmetry breaking of cellular mechanics in order to facilitate tissue motion and model epithelial tissue. We propose that their functions may be evolutionarily conserved in tubular/acinar vertebrate organs.</p></div

Fat2 locally both directs and reinforces Myo-II in individual follicle cells to promote epithelial rotation.

<p><b>(A)</b> Angular correction approach (Material and Methods). Time-projected MRLC::GFP example of the angularly corrected image of <i>fat2</i> mutant follicle cells. A = anterior, P = posterior. <b>(B)</b> First row: Angular distribution and fractions of MRLC::GFP movements as described (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007107#pgen.1007107.g001" target="_blank">Fig 1</a>) for the angularly corrected (Material and Methods) stage 4 (slow epithelial rotation) and <i>fat2</i> mutant stage 7 (no epithelial rotation). Second row: Frequencies of MRLC::GFP movements for individual egg chambers after angular correction, in four quadrants (see description in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007107#pgen.1007107.g001" target="_blank">Fig 1</a>) with <i>P-</i>values < 0.001 (***) shown. Last panel: Frequencies of MRLC::GFP movement in Up and Down quadrants as a readout for Myo-II symmetry breaking in control stage 4 and the angularly corrected <i>fat2</i> mutant stage 7. A = asymmetry (black = strong, grey = weak), S = symmetry. <b>(C)</b> First row: Weighted ratios of MRLC::GFP moving against (retrograde) and with (anterograde) the direction of epithelial rotation, plotted on a <i>log2</i> scale. Dots represent individual follicle cells and colour individual egg chambers (EC). Box plots with median are shown. Symmetry border is at 0 (red line). Note that MRLC::GFP prefers to move mainly in a retrograde direction in individual follicle cells during rotation initiation (control stage 1/2) and fast epithelial rotation (control stage 7) in contrast to no epithelial rotation (stage 1/2 and stage 7) and slow epithelial rotation (stage 4) where a few cells also show anterograde MRLC::GFP movement. Second row: Frequencies of binned MRLC::GFP ratios over analyzed egg chambers and types of epithelial rotation are shown. <b>(D)</b> Ratios of MRLC::GFP, moving against (retrograde) and with (anterograde) the direction of epithelial rotation, analyzed in individual follicle cells of small <i>fat2</i> mutant clones (lack of green nuclei, Material and Methods) and their control neighbours (green nuclei) are plotted on a <i>log₂</i> scale. The number of analyzed MRLC::GFP signals is indicated in red (number of analyzed follicle cells/egg chambers is shown in brackets). Coloured stars in images indicate the direction of epithelial rotation. Time and <i>P-</i>value < 0.001 (***) are shown. Scale bar = 5μm. Anterior is on the left.</p

Epithelial rotation is required for the directed elongation of follicle cells.

<p><b>(A)</b> Comparison of roundness parameter (Material and Methods) of follicle cells with different migratory speed: slow migrating follicle cells (control stage 4), fast migrating follicle cells (control stage 7), follicle cells in the static follicle epithelium (<i>fat2</i> mutant follicle cells), follicle cells depleted for actin, Latrunculin A and depleted for Arp2/3 complex, CK-666, migrating <i>fat2</i> mutant follicle cells in small clones and their migrating control neighbours (in yellow panel) and follicle cells with accelerated migration (<i>mys</i> heterozygous mutants). *** = <i>P</i><0.001, * = <i>P</i><0.05. Note that the roundness parameter of analyzed categories was statistically compared to the one with no indicated stars. Black <i>P</i>-values indicate how the roundness parameter differs from the control stage 7 (fast epithelial rotation). Red <i>P</i>-values show how the roundness parameter differs from the clonal control stage 7/8 (fast epithelial rotation in the <i>fat2</i> mutant mosaic eggs chambers). <b>(B)</b> Angular distribution of alignment of cell elongation and of MRLC::GFP movement expressed as frequencies in 20°-bin-rose diagrams are shown for slow (control stage 4), fast (control stage 7) and no (<i>fat2</i> mutant of stage 7) epithelial rotation. Yellow bars show the direction of follicle cell elongation and berry-coloured lines the direction of local Myo-II in the range of 0°-180°. Scale bars = 5μm. Anterior is on the left.</p

Modelling planar polarity of epithelia: the role of signal relay in collective cell polarization

Collective cell polarization is an important characteristic of tissues. Epithelia commonly display cellular structures that are polarized within the plane of the tissue. Establishment of this planar cell polarity requires mechanisms that locally align polarized structures between neighbouring cells, as well as cues that provide global information about alignment relative to an axis of a tissue. In the Drosophila ovary, the cadherin Fat2 is required to orient actin filaments located at the basal side of follicle cells perpendicular to the long axis of the egg chamber. The mechanisms directing this orientation of actin filaments, however, remain unknown. Here we show, using genetic mosaic analysis, that fat2 is not essential for the local alignment of actin filaments between neighbouring cells. Moreover, we provide evidence that Fat2 is involved in the propagation of a cue specifying the orientation of actin filaments relative to the tissue axis. Monte Carlo simulations of actin filament orientation resemble the results of the genetic mosaic analysis, if it is assumed that a polarity signal can propagate from a signal source only through a connected chain of wild-type cells. Our results suggest that Fat2 is required for propagating global polarity information within the follicle epithelium through direct cell–cell contact. Our computational model might be more generally applicable to study collective cell polarization in tissues