<i>Embryo defective 14</i> encodes a plastid‐targeted <scp>cGTP</scp>ase essential for embryogenesis in maize

Li, Cuiling; Shen, Yun; Meeley, Robert B.; McCarty, Donald R.; Tan, Bin

doi:10.1111/tpj.13045

Cited by 24 publications

(16 citation statements)

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“…S3 ). In these respects, duf177a has a typical maize emb phenotype as described in previous studies ( Clark and Sheridan, 1991 ; Ma and Dooner, 2004 ; Magnard et al , 2004 ; Sosso et al , 2012 ; Shen et al , 2013 ; Zhang et al , 2013 ; Li et al , 2015 ).…”

Section: Resultssupporting

confidence: 71%

“…These results indicated that duf177a mutant embryos do not progress beyond the early transition stage of embryogenesis. In this respect, the duf177a phenotype is similar to an emerging class of maize emb mutants implicated in disruption of plastid gene expression ( Ma and Dooner, 2004 ; Magnard et al , 2004 ; Sosso et al , 2012 ; Shen et al , 2013 ; Zhang et al , 2013 ; Li et al , 2015 ). In maize, the emb phenotypes of plastid gene expression mutants are suppressed in certain inbred backgrounds to condition an albino seedling phenotype ( Sosso et al , 2012 ; Zhang et al , 2013 ).…”

Section: Resultsmentioning

confidence: 83%

“…In certain non-permissive genetic backgrounds (e.g. W22 inbred), mutations in the nuclear-encoded plastid ribosomal proteins, PRPL35 ( Magnard et al , 2004 ) and PRPS9 ( lem1 ; Ma and Dooner, 2004 ); PPR8522 ( emb8522 ; Sosso et al , 2012 ); plastid translation initiation factor ( tif3 ; Shen et al , 2013 ); plastid ribosome assembly regulator, WHIRLY1 ( why1 ; Zhang et al , 2013 ); and EMB14 ( emb14 ; Li et al , 2015 ) uniformly block embryo development at an early transition stage. In contrast, in the permissive B73 inbred background, the emb phenotypes of emb8522 , tif3 , why1 , and emb14 mutants are suppressed ( Sosso et al , 2012 ; Zhang et al , 2013 ) to condition an albino seedling phenotype.…”

Section: Introductionmentioning

confidence: 99%

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Essential role of conserved DUF177A protein in plastid 23S rRNA accumulation and plant embryogenesis

Yang¹,

Suzuki²,

McCarty³

2016

Journal of Experimental Botany

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Section: Resultssupporting

confidence: 71%

Section: Resultsmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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Essential role of conserved DUF177A protein in plastid 23S rRNA accumulation and plant embryogenesis

Yang¹,

Suzuki²,

McCarty³

2016

Journal of Experimental Botany

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“…Notably, the Arabidopsis GCD ortholog has not been implicated in embryo patterning . In maize, a large class of mutants defective in plastid protein translation arrest embryogenesis at the transition stage (Magnard et al, 2004;Shen et al, 2013;Li et al, 2015;Yang et al, 2016) although it is not clear whether these genes have a direct role in controlling polarization of the embryo. Other investigations of patterning mechanisms during early embryogenesis in maize have largely relied on analysis of orthologs of Arabidopsis genes implicated in embryogenesis and polar auxin transport (Nardmann et al, 2007;Zimmermann and Werr, 2007;Chandler et al, 2008;Forestan et al, 2010;Chen et al, 2014).…”

Section: Shai1 Is Required For Proper Patterning and Organ Differentimentioning

confidence: 99%

Autonomous and non‐autonomous functions of the maize Shohai1 gene, encoding a RWP‐RK putative transcription factor, in regulation of embryo and endosperm development

Mimura

Kudo

et al. 2018

The Plant Journal

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In plants, establishment of the basic body plan during embryogenesis involves complex processes of axis formation, cell fate specification and organ differentiation. While molecular mechanisms of embryogenesis have been well studied in the eudicot Arabidopsis, only a small number of genes regulating embryogenesis has been identified in grass species. Here, we show that a RKD-type RWP-RK transcription factor encoded by Shohai1 (Shai1) is indispensable for embryo and endosperm development in maize. Loss of Shai1 function causes variable morphological defects in the embryo including small scutellum, shoot axis bifurcation and arrest during early organogenesis. Analysis of molecular markers in mutant embryos reveals disturbed patterning of gene expression and altered polar auxin transport. In contrast with typical embryo-defective (emb) mutants that expose a vacant embryo pocket in the endosperm, the endosperm of shai1 kernels conforms to the varied size and shape of the embryo. Furthermore, genetic analysis confirms that Shai1 is required for autonomous formation of the embryo pocket in endosperm of emb mutants. Analyses of genetic mosaic kernels generated by B-A translocation revealed that expression of Shai1 in the endosperm could partially rescue a shai1 mutant embryo and suggested that Shai1 is involved in non-cell autonomous signaling from endosperm that supports normal embryo growth. Taken together, we propose that the Shai1 gene functions in regulating embryonic patterning during grass embryogenesis partly by endosperm-to-embryo interaction.

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“…On the other hand, many genes controlling maize kernel development have been cloned using kernel mutants identified from Robertson's Mutator stocks, including emp2 (empty pericarp2), emp4, emp5, emp16, dek1 (defective kernel1), dek35, maize pentatricopeptide repeat6, small kernel1, embryo defective14, U6 biogenesis-like1, and many others (Fu et al, 2002;Lid et al, 2002;Gutiérrez-Marcos et al, 2007;Manavski et al, 2012;Liu et al, 2013;Li et al, 2014Li et al, , 2015Chen et al, 2016;Xiu et al, 2016). Mutations in these genes usually have severe phenotypes in kernels, such as empty pericarp, where both embryo and endosperm cannot develop properly.…”

mentioning

confidence: 99%

The Conserved and Unique Genetic Architecture of Kernel Size and Weight in Maize and Rice

et al. 2017

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Maize (Zea mays) is a major staple crop. Maize kernel size and weight are important contributors to its yield. Here, we measured kernel length, kernel width, kernel thickness, hundred kernel weight, and kernel test weight in 10 recombinant inbred line populations and dissected their genetic architecture using three statistical models. In total, 729 quantitative trait loci (QTLs) were identified, many of which were identified in all three models, including 22 major QTLs that each can explain more than 10% of phenotypic variation. To provide candidate genes for these QTLs, we identified 30 maize genes that are orthologs of 18 rice (Oryza sativa) genes reported to affect rice seed size or weight. Interestingly, 24 of these 30 genes are located in the identified QTLs or within 1 Mb of the significant single-nucleotide polymorphisms. We further confirmed the effects of five genes on maize kernel size/weight in an independent association mapping panel with 540 lines by candidate gene association analysis. Lastly, the function of ZmINCW1, a homolog of rice GRAIN INCOMPLETE FILLING1 that affects seed size and weight, was characterized in detail. ZmINCW1 is close to QTL peaks for kernel size/weight (less than 1 Mb) and contains significant single-nucleotide polymorphisms affecting kernel size/weight in the association panel. Overexpression of this gene can rescue the reduced weight of the Arabidopsis (Arabidopsis thaliana) homozygous mutant line in the AtcwINV2 gene (Arabidopsis ortholog of ZmINCW1). These results indicate that the molecular mechanisms affecting seed development are conserved in maize, rice, and possibly Arabidopsis.Maize (Zea mays) is one of the most important crops and is cultivated worldwide as a source of staple food, animal feed, and industrial materials. According to the Food and Agriculture Organization, the production of maize was 1,016.7 million tons in 2013, which was far more than rice (Oryza sativa) and wheat (Triticum aestivum; 745.7 and 713.1 million tons, respectively). Yield improvement is a central goal of maize breeding. Kernel size and weight are two significant components of maize yield, and many attempts have been made to elucidate the genetic basis of kernel size and weight.Many studies have mapped quantitative trait loci (QTLs) for natural variations in kernel size and weight. (2015) mapped 28 QTLs in a test cross population. Most of these studies used two diverse inbred lines to develop the segregating population and used a limited number of genetic markers to construct the linkage map, which greatly limited the resolution and power to detect rare and/or small-effect QTLs. Large-scale QTL mapping studies including more diverse genetic backgrounds and dense genetic markers would provide more insight into the number and effect of QTLs controlling the natural variations of kernel size and weight in maize.

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Embryo defective 14 encodes a plastid‐targeted cGTPase essential for embryogenesis in maize

Cited by 24 publications

References 73 publications

Essential role of conserved DUF177A protein in plastid 23S rRNA accumulation and plant embryogenesis

Essential role of conserved DUF177A protein in plastid 23S rRNA accumulation and plant embryogenesis

Autonomous and non‐autonomous functions of the maize Shohai1 gene, encoding a RWP‐RK putative transcription factor, in regulation of embryo and endosperm development

The Conserved and Unique Genetic Architecture of Kernel Size and Weight in Maize and Rice

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