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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

Reciprocal crosses between Lxm1/+ and wild-type siblings. Black arrowheads point to miniature kernels. (A)Lxm1/+ female with mild leaf phenotype crossed by wild-type male. (B) Enlargement of boxed region in (A). White arrowhead points to a kernel with a loose pericarp. (C) Wild-type female crossed by Lxm1/+ male with mild leaf phenotype. (D)Lxm1/+ female with strong leaf phenotype crossed by wild-type male. Arrow points to an aborted kernel. (E) Wild-type female crossed by Lxm1/+ male with strong leaf phenotype. (F) Frequency of abnormal kernel types in reciprocal crosses between Lxm1-O or Lxm-N2530 heterozygotes and homozygous wild type. Female genotypes are listed first.
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Figure 6: Reciprocal crosses between Lxm1/+ and wild-type siblings. Black arrowheads point to miniature kernels. (A)Lxm1/+ female with mild leaf phenotype crossed by wild-type male. (B) Enlargement of boxed region in (A). White arrowhead points to a kernel with a loose pericarp. (C) Wild-type female crossed by Lxm1/+ male with mild leaf phenotype. (D)Lxm1/+ female with strong leaf phenotype crossed by wild-type male. Arrow points to an aborted kernel. (E) Wild-type female crossed by Lxm1/+ male with strong leaf phenotype. (F) Frequency of abnormal kernel types in reciprocal crosses between Lxm1-O or Lxm-N2530 heterozygotes and homozygous wild type. Female genotypes are listed first.

Mentions: Heterozygotes for both Lxm mutations also produce miniature seeds of different severity and frequency depending upon the direction of the cross (Figure 6). Lxm1-O/+ and Lxm*-N2530/+ females segregate kernels that are small and pale with a loose pericarp. Progeny testing of kernels from crosses of Lxm/+ females by homozygous wild-type males revealed that inheritance of the mutation (i.e., the fertilization of mutant embryo sacs) is correlated with the miniature kernel phenotype (19/21 miniatures that were tested had inherited Lxm but only 2/31 normal kernels tested had inherited Lxm). Although the crosses of Lxm/+ males onto wild type do not produce the reduced endosperm, loose pericarp class of kernels, some crosses do produce a less severe miniature kernel type (Figure 6E), particularly in crosses using Lxm plants with the most severe leaf phenotype. When crossed as females, these severe Lxm heterozygotes produce some miniatures and some early aborting kernels and have partial sterility (Figure 6D). All abnormal kernel types are more common in crosses with Lxm females than males, especially the most severe classes (Figure 6F). The loose pericarp and aborted kernel phenotypes are rarely seen in crosses with Lxm1-O or Lxm*-N2530 males but are found in females of both mutants.


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

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

Reciprocal crosses between Lxm1/+ and wild-type siblings. Black arrowheads point to miniature kernels. (A)Lxm1/+ female with mild leaf phenotype crossed by wild-type male. (B) Enlargement of boxed region in (A). White arrowhead points to a kernel with a loose pericarp. (C) Wild-type female crossed by Lxm1/+ male with mild leaf phenotype. (D)Lxm1/+ female with strong leaf phenotype crossed by wild-type male. Arrow points to an aborted kernel. (E) Wild-type female crossed by Lxm1/+ male with strong leaf phenotype. (F) Frequency of abnormal kernel types in reciprocal crosses between Lxm1-O or Lxm-N2530 heterozygotes and homozygous wild type. Female genotypes are listed first.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 6: Reciprocal crosses between Lxm1/+ and wild-type siblings. Black arrowheads point to miniature kernels. (A)Lxm1/+ female with mild leaf phenotype crossed by wild-type male. (B) Enlargement of boxed region in (A). White arrowhead points to a kernel with a loose pericarp. (C) Wild-type female crossed by Lxm1/+ male with mild leaf phenotype. (D)Lxm1/+ female with strong leaf phenotype crossed by wild-type male. Arrow points to an aborted kernel. (E) Wild-type female crossed by Lxm1/+ male with strong leaf phenotype. (F) Frequency of abnormal kernel types in reciprocal crosses between Lxm1-O or Lxm-N2530 heterozygotes and homozygous wild type. Female genotypes are listed first.
Mentions: Heterozygotes for both Lxm mutations also produce miniature seeds of different severity and frequency depending upon the direction of the cross (Figure 6). Lxm1-O/+ and Lxm*-N2530/+ females segregate kernels that are small and pale with a loose pericarp. Progeny testing of kernels from crosses of Lxm/+ females by homozygous wild-type males revealed that inheritance of the mutation (i.e., the fertilization of mutant embryo sacs) is correlated with the miniature kernel phenotype (19/21 miniatures that were tested had inherited Lxm but only 2/31 normal kernels tested had inherited Lxm). Although the crosses of Lxm/+ males onto wild type do not produce the reduced endosperm, loose pericarp class of kernels, some crosses do produce a less severe miniature kernel type (Figure 6E), particularly in crosses using Lxm plants with the most severe leaf phenotype. When crossed as females, these severe Lxm heterozygotes produce some miniatures and some early aborting kernels and have partial sterility (Figure 6D). All abnormal kernel types are more common in crosses with Lxm females than males, especially the most severe classes (Figure 6F). The loose pericarp and aborted kernel phenotypes are rarely seen in crosses with Lxm1-O or Lxm*-N2530 males but are found in females of both mutants.

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