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Correlation between a loss of auxin signaling and a loss of proliferation in maize antipodal cells.

Chettoor AM, Evans MM - Front Plant Sci (2015)

Bottom Line: In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells.Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells.The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Biology, Carnegie Institution for Science Stanford, CA USA.

ABSTRACT
The plant life cycle alternates between two genetically active generations: the diploid sporophyte and the haploid gametophyte. In angiosperms the gametophytes are sexually dimorphic and consist of only a few cells. The female gametophyte, or embryo sac, is comprised of four cell types: two synergids, an egg cell, a central cell, and a variable number of antipodal cells. In some species the antipodal cells are indistinct and fail to proliferate, so many aspects of antipodal cell function and development have been unclear. In maize and many other grasses, the antipodal cells proliferate to produce a highly distinct cluster at the chalazal end of the embryo sac that persists at the apex of the endosperm after fertilization. The antipodal cells are a site of auxin accumulation in the maize embryo sac. Analysis of different families of genes involved in auxin biosynthesis, distribution, and signaling for expression in the embryo sac demonstrates that all steps are expressed within the embryo sac. In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells. Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells. The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells.

No MeSH data available.


Related in: MedlinePlus

Effect of Lxm mutations on embryo sac development. (A–D) Embryo sacs from a Lxm1-O/+; W23 heterozygote fixed in FAA and stained with Acriflavine and Propidium Iodide and (E–H) Embryo sacs from a Lxm*-N2530 heterozygote in a hybrid genetic background fixed in FAA. (A,B,E,F) Embryo sacs with abnormal antipodal cell clusters. (C,D,G,H) Normal sibling embryo sacs for each mutant line. (B,D,F,H) are magnifications of the antipodal cells in (A,C,E,G), respectively. Arrows indicate antipodal cell cluster. Scale bar = 100 μm (A,C,E,G) and = 33 μm (B,D,F,H).
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Figure 5: Effect of Lxm mutations on embryo sac development. (A–D) Embryo sacs from a Lxm1-O/+; W23 heterozygote fixed in FAA and stained with Acriflavine and Propidium Iodide and (E–H) Embryo sacs from a Lxm*-N2530 heterozygote in a hybrid genetic background fixed in FAA. (A,B,E,F) Embryo sacs with abnormal antipodal cell clusters. (C,D,G,H) Normal sibling embryo sacs for each mutant line. (B,D,F,H) are magnifications of the antipodal cells in (A,C,E,G), respectively. Arrows indicate antipodal cell cluster. Scale bar = 100 μm (A,C,E,G) and = 33 μm (B,D,F,H).

Mentions: To determine a potential function for the auxin maximum in the antipodal cells, we then examined the effect of an antipodal cell mutant on the expression of the DR5 and PIN1 fluorescent reporters. Because the indeterminate gametophyte1 (ig1) mutation affects both leaf polarity and embryo sac development (Evans, 2007), other leaf polarity mutants were examined for effects on embryo sac morphology. The Laxmidrib1-O (Lxm1-O) mutant is a dominant mutant with adaxialized leaves. Sectors of adaxial tissue are produced on the abaxial side of leaves with ectopic leaf flaps produced on either side of these sectors (the opposite leaf polarity defect as ig1) (Schichnes et al., 1997; Schichnes and Freeling, 1998). Approximately one third of the embryo sacs in Lxm1-O/+ heterozygotes in a W23 inbred background are abnormal (39/122) (Figure 5). These embryo sacs have fewer antipodal cells than their wild-type siblings (six antipodal cell nuclei in Figures 5A,B), indicating that proliferation of the antipodal cells in mutant embryo sacs is reduced or in some cases absent. The size and morphology of these antipodal cells are similar to wild type, however, and, like wild type, the nuclei have speckled staining with Propidium Iodide and lack prominent nucleoli. The overall size and morphology of the central cell, egg cell, and synergids are not affected by Lxm1-O. A second mutation, Lxm*-N2530, which has similar effects on leaf development as Lxm1-O, also produces embryo sacs with smaller antipodal cell clusters than wild type, supporting the argument that this is a result of the Lxm mutations rather than a second mutation segregating in the background (Figures 5E–H). The normal and mutant antipodal cells of the Lxm*-N2530 line are slightly larger and more vacuolated than those of the Lxm1-O line, but these mutations are in different inbred backgrounds.


Correlation between a loss of auxin signaling and a loss of proliferation in maize antipodal cells.

Chettoor AM, Evans MM - Front Plant Sci (2015)

Effect of Lxm mutations on embryo sac development. (A–D) Embryo sacs from a Lxm1-O/+; W23 heterozygote fixed in FAA and stained with Acriflavine and Propidium Iodide and (E–H) Embryo sacs from a Lxm*-N2530 heterozygote in a hybrid genetic background fixed in FAA. (A,B,E,F) Embryo sacs with abnormal antipodal cell clusters. (C,D,G,H) Normal sibling embryo sacs for each mutant line. (B,D,F,H) are magnifications of the antipodal cells in (A,C,E,G), respectively. Arrows indicate antipodal cell cluster. Scale bar = 100 μm (A,C,E,G) and = 33 μm (B,D,F,H).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4374392&req=5

Figure 5: Effect of Lxm mutations on embryo sac development. (A–D) Embryo sacs from a Lxm1-O/+; W23 heterozygote fixed in FAA and stained with Acriflavine and Propidium Iodide and (E–H) Embryo sacs from a Lxm*-N2530 heterozygote in a hybrid genetic background fixed in FAA. (A,B,E,F) Embryo sacs with abnormal antipodal cell clusters. (C,D,G,H) Normal sibling embryo sacs for each mutant line. (B,D,F,H) are magnifications of the antipodal cells in (A,C,E,G), respectively. Arrows indicate antipodal cell cluster. Scale bar = 100 μm (A,C,E,G) and = 33 μm (B,D,F,H).
Mentions: To determine a potential function for the auxin maximum in the antipodal cells, we then examined the effect of an antipodal cell mutant on the expression of the DR5 and PIN1 fluorescent reporters. Because the indeterminate gametophyte1 (ig1) mutation affects both leaf polarity and embryo sac development (Evans, 2007), other leaf polarity mutants were examined for effects on embryo sac morphology. The Laxmidrib1-O (Lxm1-O) mutant is a dominant mutant with adaxialized leaves. Sectors of adaxial tissue are produced on the abaxial side of leaves with ectopic leaf flaps produced on either side of these sectors (the opposite leaf polarity defect as ig1) (Schichnes et al., 1997; Schichnes and Freeling, 1998). Approximately one third of the embryo sacs in Lxm1-O/+ heterozygotes in a W23 inbred background are abnormal (39/122) (Figure 5). These embryo sacs have fewer antipodal cells than their wild-type siblings (six antipodal cell nuclei in Figures 5A,B), indicating that proliferation of the antipodal cells in mutant embryo sacs is reduced or in some cases absent. The size and morphology of these antipodal cells are similar to wild type, however, and, like wild type, the nuclei have speckled staining with Propidium Iodide and lack prominent nucleoli. The overall size and morphology of the central cell, egg cell, and synergids are not affected by Lxm1-O. A second mutation, Lxm*-N2530, which has similar effects on leaf development as Lxm1-O, also produces embryo sacs with smaller antipodal cell clusters than wild type, supporting the argument that this is a result of the Lxm mutations rather than a second mutation segregating in the background (Figures 5E–H). The normal and mutant antipodal cells of the Lxm*-N2530 line are slightly larger and more vacuolated than those of the Lxm1-O line, but these mutations are in different inbred backgrounds.

Bottom Line: In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells.Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells.The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Biology, Carnegie Institution for Science Stanford, CA USA.

ABSTRACT
The plant life cycle alternates between two genetically active generations: the diploid sporophyte and the haploid gametophyte. In angiosperms the gametophytes are sexually dimorphic and consist of only a few cells. The female gametophyte, or embryo sac, is comprised of four cell types: two synergids, an egg cell, a central cell, and a variable number of antipodal cells. In some species the antipodal cells are indistinct and fail to proliferate, so many aspects of antipodal cell function and development have been unclear. In maize and many other grasses, the antipodal cells proliferate to produce a highly distinct cluster at the chalazal end of the embryo sac that persists at the apex of the endosperm after fertilization. The antipodal cells are a site of auxin accumulation in the maize embryo sac. Analysis of different families of genes involved in auxin biosynthesis, distribution, and signaling for expression in the embryo sac demonstrates that all steps are expressed within the embryo sac. In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells. Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells. The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells.

No MeSH data available.


Related in: MedlinePlus