Limits...
Ectopic shoot meristem generation in monocotyledonous rpk1 mutants is linked to SAM loss and altered seedling morphology.

Fiesselmann BS, Luichtl M, Yang X, Matthes M, Peis O, Torres-Ruiz RA - BMC Plant Biol. (2015)

Bottom Line: In strong rpk1 alleles, about 10 % of these (i. e. 1 % of all homozygotes) did not develop a SAM.The results highlight the developmental autonomy of the SAM vs. cotyledons and suggest that the primary rpk1 defect does not lie in the seedling's ability to express SAM genes or to develop a shoot meristem.The specific cotyledon defect in rpk1 mutants thus sheds light upon the developmental implications of the transition from two cotyledons to one.

View Article: PubMed Central - PubMed

Affiliation: Lehrstuhl für Genetik, Technische Universität München, Wissenschaftszentrum Weihenstephan, Emil-Ramann-Str. 8, D-85354, Freising, Germany. birgit.fiesselmann@gmail.com.

ABSTRACT

Background: In dicot Arabidopsis thaliana embryos two cotyledons develop largely autonomously from the shoot apical meristem (SAM). Recessive mutations in the Arabidopsis receptor-like kinase RPK1 lead to monocotyledonous seedlings, with low (10 %) penetrance due to complex functional redundancy. In strong rpk1 alleles, about 10 % of these (i. e. 1 % of all homozygotes) did not develop a SAM. We wondered whether RPK1 might also control SAM gene expression and SAM generation in addition to its known stochastic impact on cell division and PINFORMED1 (PIN1) polarity in the epidermis.

Results: SAM-less seedlings developed a simple morphology with a straight and continuous hypocotyl-cotyledon structure lacking a recognizable epicotyl. According to rpk1's auxin-related PIN1 defect, the seedlings displayed defects in the vascular tissue. Surprisingly, SAM-less seedlings variably expressed essential SAM specific genes along the hypocotyl-cotyledon structure up into the cotyledon lamina. Few were even capable of developing an ectopic shoot meristem (eSM) on top of the cotyledon.

Conclusions: The results highlight the developmental autonomy of the SAM vs. cotyledons and suggest that the primary rpk1 defect does not lie in the seedling's ability to express SAM genes or to develop a shoot meristem. Rather, rpk1's known defects in cell division and auxin homeostasis, by disturbed PIN1 polarity, impact on SAM and organ generation. In early embryo stages this failure generates a simplified monocotyledonous morphology. Once generated, this likely entails a loss of positional information that in turn affects the spatiotemporal development of the SAM. SAM-bearing and SAM-less monocotyledonous phenotypes show morphological similarities either to real monocots or to dicot species, which only develop one cotyledon. The specific cotyledon defect in rpk1 mutants thus sheds light upon the developmental implications of the transition from two cotyledons to one.

No MeSH data available.


Related in: MedlinePlus

Meristem structure and size of monocot rpk1-7 seedlings. a Median section of a seedling with SAM and insets showing a magnified series of sections through the SAM (that of the median section is framed). Stomata are separated by other epidermal cells (arrowheads). Note the seemingly terminal position of the cotyledon, while the vascular elements demonstrate a lateral origin. b An eSM seedling (left). Insets show magnifications with details (right): irregularly spaced stomata (top, arrowheads); a regularly shaped meristem with leaf primordia (middle); a further section few microns apart from the former (bottom). Arrows point towards the root. Scale bars: 100 μm (left parts of a and b) and 20 μm (insets). c Means and SDs of rpk1-7 seedlings with one, two irregularly sized and two normal cotyledons and of wild-type and the clv3 mutant respectively (brackets: numbers of seedlings analysed). d Representatives of the different seedlings (except irregular seedlings)
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4492102&req=5

Fig3: Meristem structure and size of monocot rpk1-7 seedlings. a Median section of a seedling with SAM and insets showing a magnified series of sections through the SAM (that of the median section is framed). Stomata are separated by other epidermal cells (arrowheads). Note the seemingly terminal position of the cotyledon, while the vascular elements demonstrate a lateral origin. b An eSM seedling (left). Insets show magnifications with details (right): irregularly spaced stomata (top, arrowheads); a regularly shaped meristem with leaf primordia (middle); a further section few microns apart from the former (bottom). Arrows point towards the root. Scale bars: 100 μm (left parts of a and b) and 20 μm (insets). c Means and SDs of rpk1-7 seedlings with one, two irregularly sized and two normal cotyledons and of wild-type and the clv3 mutant respectively (brackets: numbers of seedlings analysed). d Representatives of the different seedlings (except irregular seedlings)

Mentions: A plant with an eSM was histologically compared with a “normal“ monocot seedling (Fig 3). The latter developed a SAM at the base of the cotyledon, which harboured regular cell files belonging to epidermis, palisade, mesophyll and xylem/phloem tissue, very much like a SAM of a dicot seedling. Within all tissues, the cells showed regular cell size proportions and vacuolation. Stomata were found above small cavities and were well separated from each other by epidermal cells (Fig. 3a). The SAM was positioned at the base of the remaining cotyledon where it would be normally expected. Its organization consisted of a group of small densely stained cells, which laterally gave rise to leaf primordia (Fig. 3a). As seen from the vascular system, the origin of the cotyledon is lateral and not terminal.Fig. 3


Ectopic shoot meristem generation in monocotyledonous rpk1 mutants is linked to SAM loss and altered seedling morphology.

Fiesselmann BS, Luichtl M, Yang X, Matthes M, Peis O, Torres-Ruiz RA - BMC Plant Biol. (2015)

Meristem structure and size of monocot rpk1-7 seedlings. a Median section of a seedling with SAM and insets showing a magnified series of sections through the SAM (that of the median section is framed). Stomata are separated by other epidermal cells (arrowheads). Note the seemingly terminal position of the cotyledon, while the vascular elements demonstrate a lateral origin. b An eSM seedling (left). Insets show magnifications with details (right): irregularly spaced stomata (top, arrowheads); a regularly shaped meristem with leaf primordia (middle); a further section few microns apart from the former (bottom). Arrows point towards the root. Scale bars: 100 μm (left parts of a and b) and 20 μm (insets). c Means and SDs of rpk1-7 seedlings with one, two irregularly sized and two normal cotyledons and of wild-type and the clv3 mutant respectively (brackets: numbers of seedlings analysed). d Representatives of the different seedlings (except irregular seedlings)
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4492102&req=5

Fig3: Meristem structure and size of monocot rpk1-7 seedlings. a Median section of a seedling with SAM and insets showing a magnified series of sections through the SAM (that of the median section is framed). Stomata are separated by other epidermal cells (arrowheads). Note the seemingly terminal position of the cotyledon, while the vascular elements demonstrate a lateral origin. b An eSM seedling (left). Insets show magnifications with details (right): irregularly spaced stomata (top, arrowheads); a regularly shaped meristem with leaf primordia (middle); a further section few microns apart from the former (bottom). Arrows point towards the root. Scale bars: 100 μm (left parts of a and b) and 20 μm (insets). c Means and SDs of rpk1-7 seedlings with one, two irregularly sized and two normal cotyledons and of wild-type and the clv3 mutant respectively (brackets: numbers of seedlings analysed). d Representatives of the different seedlings (except irregular seedlings)
Mentions: A plant with an eSM was histologically compared with a “normal“ monocot seedling (Fig 3). The latter developed a SAM at the base of the cotyledon, which harboured regular cell files belonging to epidermis, palisade, mesophyll and xylem/phloem tissue, very much like a SAM of a dicot seedling. Within all tissues, the cells showed regular cell size proportions and vacuolation. Stomata were found above small cavities and were well separated from each other by epidermal cells (Fig. 3a). The SAM was positioned at the base of the remaining cotyledon where it would be normally expected. Its organization consisted of a group of small densely stained cells, which laterally gave rise to leaf primordia (Fig. 3a). As seen from the vascular system, the origin of the cotyledon is lateral and not terminal.Fig. 3

Bottom Line: In strong rpk1 alleles, about 10 % of these (i. e. 1 % of all homozygotes) did not develop a SAM.The results highlight the developmental autonomy of the SAM vs. cotyledons and suggest that the primary rpk1 defect does not lie in the seedling's ability to express SAM genes or to develop a shoot meristem.The specific cotyledon defect in rpk1 mutants thus sheds light upon the developmental implications of the transition from two cotyledons to one.

View Article: PubMed Central - PubMed

Affiliation: Lehrstuhl für Genetik, Technische Universität München, Wissenschaftszentrum Weihenstephan, Emil-Ramann-Str. 8, D-85354, Freising, Germany. birgit.fiesselmann@gmail.com.

ABSTRACT

Background: In dicot Arabidopsis thaliana embryos two cotyledons develop largely autonomously from the shoot apical meristem (SAM). Recessive mutations in the Arabidopsis receptor-like kinase RPK1 lead to monocotyledonous seedlings, with low (10 %) penetrance due to complex functional redundancy. In strong rpk1 alleles, about 10 % of these (i. e. 1 % of all homozygotes) did not develop a SAM. We wondered whether RPK1 might also control SAM gene expression and SAM generation in addition to its known stochastic impact on cell division and PINFORMED1 (PIN1) polarity in the epidermis.

Results: SAM-less seedlings developed a simple morphology with a straight and continuous hypocotyl-cotyledon structure lacking a recognizable epicotyl. According to rpk1's auxin-related PIN1 defect, the seedlings displayed defects in the vascular tissue. Surprisingly, SAM-less seedlings variably expressed essential SAM specific genes along the hypocotyl-cotyledon structure up into the cotyledon lamina. Few were even capable of developing an ectopic shoot meristem (eSM) on top of the cotyledon.

Conclusions: The results highlight the developmental autonomy of the SAM vs. cotyledons and suggest that the primary rpk1 defect does not lie in the seedling's ability to express SAM genes or to develop a shoot meristem. Rather, rpk1's known defects in cell division and auxin homeostasis, by disturbed PIN1 polarity, impact on SAM and organ generation. In early embryo stages this failure generates a simplified monocotyledonous morphology. Once generated, this likely entails a loss of positional information that in turn affects the spatiotemporal development of the SAM. SAM-bearing and SAM-less monocotyledonous phenotypes show morphological similarities either to real monocots or to dicot species, which only develop one cotyledon. The specific cotyledon defect in rpk1 mutants thus sheds light upon the developmental implications of the transition from two cotyledons to one.

No MeSH data available.


Related in: MedlinePlus