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1 ) are contributed by surrounding sporophytic tapetal cells.
2 localized to endoplasmic reticulum of anther tapetal cells.
3 ollen coat and premature degeneration of the tapetal cells.
4 lationship between the development of ml and tapetal cells.
5 densely stained cytoplasm typical of normal tapetal cells.
6 within the large cytoplasmic lipid bodies of tapetal cells.
7 inated secretory activity of the surrounding tapetal cells.
8 arietal cells then predominantly to daughter tapetal cells.
9 tenation in multivesicular endosomes in both tapetal cells and developing pollen grains as well as mo
10 me genes may be expressed in the sporophytic tapetal cells and in gametophytic tissues, they are regu
12 mutant anthers display swollen, hypertrophic tapetal cells and pollen grains, suggesting disrupted ce
13 Transgenic plants exhibited GUS activity in tapetal cells and pollen of the developing anthers indic
15 that produces excess microsporocytes, lacks tapetal cells, and abnormally maintains middle layer cel
16 siRNAs, develop short anthers with defective tapetal cells, and exhibit temperature-sensitive male fe
19 plasma membrane and secreted proteins in the tapetal cells at the free microspore stage, contributing
20 ly from the mitochondria into the cytosol of tapetal cells before the gross morphological changes ass
21 itical role in the BR-mediated regulation of tapetal cell degeneration and pollen development in Sola
27 m at different stages, using isolated single tapetal cells in which the in vivo morphology and volume
29 to suppress trans-differentiation of somatic tapetal cells into meiocytes, we find that mac1 anthers
33 ouble mutant anthers lack development of the tapetal cell layer, which accounts for the microspore ab
34 g laser capture microdissection, we analyzed tapetal cells, meiocytes and other somatic cells at seve
36 ese vacuolar inclusions were not observed in tapetal cells of double mutants of abcg26 and genes enco
37 are localized in microspore mother cells and tapetal cells of meiotic and post-meiotic stage anthers.
39 CPPR1 led to abnormal plastid development in tapetal cells, prolonged tapetal programmed cell death (
40 roduction and programmed cell death (PCD) in tapetal cells, resulting in delayed or premature tapetal
42 e differentiation of the microsporocytes and tapetal cells, suggesting that EMS1 mediates signals tha
43 morphology beginning at anther stage 4, with tapetal cells that have excess and/or enlarged vacuoles
44 ail to elongate, and there are fewer, larger tapetal cells that retain, rather than secrete, their co
45 ere ABCG26-exported polyketides traffic from tapetal cells to form the sporopollenin backbone, in coo
46 nsport and assembly of exine components from tapetal cells to microspores in the intact anthers of Ar
47 likely cross-link extensins to contribute to tapetal cell wall integrity during anther development.
48 asm in sunflower causes premature PCD of the tapetal cells, which then extends to other anther tissue
49 he ago1d mutant predominantly show excessive tapetal cells with little starch accumulation during pol
50 ned by biphasic protein expression in anther tapetal cells, with an initial peak around pollen meiosi
51 n, accumulated large fluorescent vacuoles in tapetal cells, with corresponding loss of fluorescence o