This study focused on the primary cell wall constituents and plasmodesmata (PD) density in three mosses and four liverwort apical cells (AC) and immediate derivatives. The three mosses have tetrahedral apical cells and the liverworts possess tetrahedral, hemidiscoid and lenticular AC geometries. The primary cell wall in the studied taxa is comprised of two layers. A fibrillar layer, which is the outer wall layer, contains compacted cellulosic fibrils, and represents the two adjacent primary walls and middle lamella, the latter of which is rarely discernible. An electron-lucent inner wall layer abuts the plasma membrane. This layer has faint fibrous materials that extend from the plasma membrane to the fibrillar layer. Generally, as the cell wall ages it thickens, the fibrillar layer increases in width while the electron-lucent wall stays more or less consistent in width. In the four liverworts, the most recent wall of the AC has the highest PD density in the apical region regardless of AC geometry. As the walls elongate, primary wall is laid down between PD, separating them and resulting in lower densities and wider PD diameters in older walls. The season of fixation and whether plants were studied from nature or culture have an influence on AC ultrastructure. A developmental study of Physcomitrella patents gametophores in four stages, bud, 2-leaved, 7-8-leaved and ~20-leaved, reveals that the primary cell wall constituents change slightly during development. Specifically, LM5 a RG-I pectin antibody against the galactan branch epitope is only localized in the fibrillar layer of young water-conducting cells in the 7-8-leaved and 20-leaved gametophores. LM20, an antibody against HG esterified pectins, does not localize in any of the cell walls during development. The distribution patterns for AGPs (JIM13 and LM2) are consistent during gametophore development and predominantly localize on the electron-lucent layer and wall/plasma membrane interface. However, LM2 is mainly localized on the fibrillar layer in 7-8-leaved cell walls. AGPs also localize on element of the cytoplasm. LM6, an antibody against an RG-I pectin with arabinan branch epitopes, also localizes AGPs and because it expressed similar distribution patterns as JIM13 and LM2 on the cell wall, it likely localizes AGP in Physcomitrella. In addition, LM6 localizes pectins on the fibrillar layer similar to LM5 and LM19 for HG unesterified pectins. Callose predominantly localizes at the PD neck region. This study provides the first documentation of changes in size and shape of AC with age in Physcomitrella patens gametophores. The PD densities of gametophytes examined in this study fall into the lineage-specific network of PD (LPD) group designated for sporophytes of monilophytes and Selaginella (heterosporous lycophyte) with single ACs. Takakia lepidozioides leafy shoot has a tetrahedral AC with a highly curved free surface. This peculiar moss has mucilage hair (MH) associated with axil of phyllids. Mucilage hair in both species are 3-celled with a forth epidermal cell as the base. However, occasional 2-celled MH is seen in T. ceratophylla. The ultrastructure of MH has similarities with other mosses and liverworts.

O cristalino de vertebrados se origina a partir da invaginação do ectoderme que recobre a vesícula óptica. A invaginação epitelial em diversos modelos é causada pela constrição celular apical, mediada pela contração apical de actina e miosina II e regulada pela GTPase RhoA. Neste trabalho nós investigamos se a invaginação do cristalino em embriões de galinha ocorre devido à constrição celular apical e se este evento é controlado por RhoA. Actina filamentosa e miosina II são expressas na porção apical do cristalino durante a invaginação. Quando a polimerização de actina é inibida por Citocalasina D, o cristalino não invagina, sugerindo que a constrição celular apical poderia contribuir para a invaginação do cristalino. RhoA também é expressa durante o desenvolvimento do cristalino, mas a inibição de RhoA, por eletroporação da forma dominante-negativo, não impediu a invaginação do placóide do cristalino, não alterou a distribuição de miosina II na porção apical do cristalino nem sua ativação, indicando que a invaginação do cristalino independe de RhoA. / Vertebrate lens derives from invagination of the ectoderm that overlies optic vesicles. Epithelial invagination in many model systems is driven by apical cell constriction, mediated by actin and myosin II contraction regulated by GTPase RhoA. Here we investigate the possibility that chick lens placode invagination could also be driven by apical cell constriction and controlled by RhoA. We show that actin and myosin II are expressed at lens apical side during lens invagination. Actin polymerization inhibition by in ovo Cytochalasin D treatment prevents lens placode invagination, suggesting that lens placode invagination could be driven by apical cell constriction. RhoA GTPase is also expressed at apical portion of lens placode and during lens invagination. However, when we overexpressed by electroporation the dominant-negative RhoA in the pre-lens ectoderm invagination was not affected. Furthermore, dominant-negative RhoA didnt affect myosin II apical localization nor myosin II phosphorilation, indicating that in lens invagination this process is not regulated by GTPase RhoA.

O cristalino de vertebrados se origina a partir da invaginação do ectoderme que recobre a vesícula óptica. A invaginação epitelial em diversos modelos é causada pela constrição celular apical, mediada pela contração apical de actina e miosina II e regulada pela GTPase RhoA. Neste trabalho nós investigamos se a invaginação do cristalino em embriões de galinha ocorre devido à constrição celular apical e se este evento é controlado por RhoA. Actina filamentosa e miosina II são expressas na porção apical do cristalino durante a invaginação. Quando a polimerização de actina é inibida por Citocalasina D, o cristalino não invagina, sugerindo que a constrição celular apical poderia contribuir para a invaginação do cristalino. RhoA também é expressa durante o desenvolvimento do cristalino, mas a inibição de RhoA, por eletroporação da forma dominante-negativo, não impediu a invaginação do placóide do cristalino, não alterou a distribuição de miosina II na porção apical do cristalino nem sua ativação, indicando que a invaginação do cristalino independe de RhoA. / Vertebrate lens derives from invagination of the ectoderm that overlies optic vesicles. Epithelial invagination in many model systems is driven by apical cell constriction, mediated by actin and myosin II contraction regulated by GTPase RhoA. Here we investigate the possibility that chick lens placode invagination could also be driven by apical cell constriction and controlled by RhoA. We show that actin and myosin II are expressed at lens apical side during lens invagination. Actin polymerization inhibition by in ovo Cytochalasin D treatment prevents lens placode invagination, suggesting that lens placode invagination could be driven by apical cell constriction. RhoA GTPase is also expressed at apical portion of lens placode and during lens invagination. However, when we overexpressed by electroporation the dominant-negative RhoA in the pre-lens ectoderm invagination was not affected. Furthermore, dominant-negative RhoA didnt affect myosin II apical localization nor myosin II phosphorilation, indicating that in lens invagination this process is not regulated by GTPase RhoA.

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