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Influence of clavata3-2 mutation on early flower development in Arabidopsis thaliana: quantitative analysis of changing geometry.

Szczesny T, Routier-Kierzkowska AL, Kwiatkowska D - J. Exp. Bot. (2008)

Bottom Line: In particular, the shape of the adaxial primordium boundary varies and seems to be related to the shape of the space available for the given primordium formation, suggesting that physical constraints play a significant role in primordium shape determination.Moreover, there is only one tunica layer in both the meristem and in the primordium until it becomes a bulge that is distinctly separated from the meristem.Starting from this stage, the anticlinal divisions predominate in subprotodermal cells, suggesting that the distribution of periclinal and anticlinal cell divisions in the early development of the flower primordium is not directly affected by the clv3-2 mutation.

View Article: PubMed Central - PubMed

Affiliation: Institute of Plant Biology, University of Wrocław, Kanonia 6/8, 50-328 Wrocław, Poland.

ABSTRACT
Early development of the flower primordium has been studied in Arabidopsis thaliana clavata3-2 (clv3-2) plants with the aid of sequential in vivo replicas and longitudinal microtome sections. Sequential replicas show that, although there is no regular phyllotaxis in the clv3-2 inflorescence shoot apex, the sites of new primordium formation are, to a large extent, predictable. The primordium always appears in a wedge-like region of the meristem periphery flanked by two older primordia. In general, stages of primordium development in clv3-2 are similar to the wild type, but quantitative geometry analysis shows that the clv3-2 primordium shape is affected even before the CLAVATA/WUSCHEL regulatory network would start to operate in the wild-type primordium. The shape of the youngest primordium in the mutant is more variable than in the wild type. In particular, the shape of the adaxial primordium boundary varies and seems to be related to the shape of the space available for the given primordium formation, suggesting that physical constraints play a significant role in primordium shape determination. The role of physical constraints is also manifested in that the shape of the primordium in the later stages, as well as the number and position of sepals, are adjusted to the available space. Longitudinal sections of clv3-2 apices show that the shape of surface cells of the meristem and young primordium is different from the wild type. Moreover, there is only one tunica layer in both the meristem and in the primordium until it becomes a bulge that is distinctly separated from the meristem. Starting from this stage, the anticlinal divisions predominate in subprotodermal cells, suggesting that the distribution of periclinal and anticlinal cell divisions in the early development of the flower primordium is not directly affected by the clv3-2 mutation.

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Central longitudinal sections of clv3-2 flower primordia at consecutive developmental stages. (A, B) Initial (lateral) bulging of the SAM periphery. (C) Upward bulging at the bottom of a shallow crease. (D, E) Bulge with a deep and sharp crease at the adaxial primordium boundary. (F, H) Bulge-shaped primordium ‘filling’ the available space between older primordia and the SAM. (I, J) Sepal formation stage. (K, L) Primordia in which stamens (St) and carpels (Ca) are formed. The flower primordia are covered by young sepals (S). The periclinal divisions in subprotodermal cells are indicated by arrows. Flower primordia are labelled with (P) and a number. Bars=30 μm.
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fig14: Central longitudinal sections of clv3-2 flower primordia at consecutive developmental stages. (A, B) Initial (lateral) bulging of the SAM periphery. (C) Upward bulging at the bottom of a shallow crease. (D, E) Bulge with a deep and sharp crease at the adaxial primordium boundary. (F, H) Bulge-shaped primordium ‘filling’ the available space between older primordia and the SAM. (I, J) Sepal formation stage. (K, L) Primordia in which stamens (St) and carpels (Ca) are formed. The flower primordia are covered by young sepals (S). The periclinal divisions in subprotodermal cells are indicated by arrows. Flower primordia are labelled with (P) and a number. Bars=30 μm.

Mentions: The consecutive stages of flower primordium formation described above, can also be recognized in the longitudinal sections. The flower primordium in the stage of the shallow crease, sectioned in a plane perpendicular to the shallow crease, is represented by P1 in Fig. 14A and B. P1 in Fig. 14C represents the stage of upward bulging at the bottom of the shallow crease or early bulge. Primordia in Fig. 14D–H are all in the bulge stage, arranged according to increasing size. They are all sectioned in the median plane. Note, that their shapes are different. Primordium P1 in Fig. 14E is nearly hemispherical. The top of P2 in Fig. 14F is flattened, unlike P2 in Fig. 14G, which is the cone with a cap. Starting from Fig. 14I the stages of flower organ initiation are represented.


Influence of clavata3-2 mutation on early flower development in Arabidopsis thaliana: quantitative analysis of changing geometry.

Szczesny T, Routier-Kierzkowska AL, Kwiatkowska D - J. Exp. Bot. (2008)

Central longitudinal sections of clv3-2 flower primordia at consecutive developmental stages. (A, B) Initial (lateral) bulging of the SAM periphery. (C) Upward bulging at the bottom of a shallow crease. (D, E) Bulge with a deep and sharp crease at the adaxial primordium boundary. (F, H) Bulge-shaped primordium ‘filling’ the available space between older primordia and the SAM. (I, J) Sepal formation stage. (K, L) Primordia in which stamens (St) and carpels (Ca) are formed. The flower primordia are covered by young sepals (S). The periclinal divisions in subprotodermal cells are indicated by arrows. Flower primordia are labelled with (P) and a number. Bars=30 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC2651453&req=5

fig14: Central longitudinal sections of clv3-2 flower primordia at consecutive developmental stages. (A, B) Initial (lateral) bulging of the SAM periphery. (C) Upward bulging at the bottom of a shallow crease. (D, E) Bulge with a deep and sharp crease at the adaxial primordium boundary. (F, H) Bulge-shaped primordium ‘filling’ the available space between older primordia and the SAM. (I, J) Sepal formation stage. (K, L) Primordia in which stamens (St) and carpels (Ca) are formed. The flower primordia are covered by young sepals (S). The periclinal divisions in subprotodermal cells are indicated by arrows. Flower primordia are labelled with (P) and a number. Bars=30 μm.
Mentions: The consecutive stages of flower primordium formation described above, can also be recognized in the longitudinal sections. The flower primordium in the stage of the shallow crease, sectioned in a plane perpendicular to the shallow crease, is represented by P1 in Fig. 14A and B. P1 in Fig. 14C represents the stage of upward bulging at the bottom of the shallow crease or early bulge. Primordia in Fig. 14D–H are all in the bulge stage, arranged according to increasing size. They are all sectioned in the median plane. Note, that their shapes are different. Primordium P1 in Fig. 14E is nearly hemispherical. The top of P2 in Fig. 14F is flattened, unlike P2 in Fig. 14G, which is the cone with a cap. Starting from Fig. 14I the stages of flower organ initiation are represented.

Bottom Line: In particular, the shape of the adaxial primordium boundary varies and seems to be related to the shape of the space available for the given primordium formation, suggesting that physical constraints play a significant role in primordium shape determination.Moreover, there is only one tunica layer in both the meristem and in the primordium until it becomes a bulge that is distinctly separated from the meristem.Starting from this stage, the anticlinal divisions predominate in subprotodermal cells, suggesting that the distribution of periclinal and anticlinal cell divisions in the early development of the flower primordium is not directly affected by the clv3-2 mutation.

View Article: PubMed Central - PubMed

Affiliation: Institute of Plant Biology, University of Wrocław, Kanonia 6/8, 50-328 Wrocław, Poland.

ABSTRACT
Early development of the flower primordium has been studied in Arabidopsis thaliana clavata3-2 (clv3-2) plants with the aid of sequential in vivo replicas and longitudinal microtome sections. Sequential replicas show that, although there is no regular phyllotaxis in the clv3-2 inflorescence shoot apex, the sites of new primordium formation are, to a large extent, predictable. The primordium always appears in a wedge-like region of the meristem periphery flanked by two older primordia. In general, stages of primordium development in clv3-2 are similar to the wild type, but quantitative geometry analysis shows that the clv3-2 primordium shape is affected even before the CLAVATA/WUSCHEL regulatory network would start to operate in the wild-type primordium. The shape of the youngest primordium in the mutant is more variable than in the wild type. In particular, the shape of the adaxial primordium boundary varies and seems to be related to the shape of the space available for the given primordium formation, suggesting that physical constraints play a significant role in primordium shape determination. The role of physical constraints is also manifested in that the shape of the primordium in the later stages, as well as the number and position of sepals, are adjusted to the available space. Longitudinal sections of clv3-2 apices show that the shape of surface cells of the meristem and young primordium is different from the wild type. Moreover, there is only one tunica layer in both the meristem and in the primordium until it becomes a bulge that is distinctly separated from the meristem. Starting from this stage, the anticlinal divisions predominate in subprotodermal cells, suggesting that the distribution of periclinal and anticlinal cell divisions in the early development of the flower primordium is not directly affected by the clv3-2 mutation.

Show MeSH
Related in: MedlinePlus