Parent-of-origin effects on seed development in Arabidopsis thaliana

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3329-3341 ◽  
Author(s):  
R.J. Scott ◽  
M. Spielman ◽  
J. Bailey ◽  
H.G. Dickinson

Many flowering plants are polyploid, but crosses between individuals of different ploidies produce seeds that develop abnormally and usually abort. Often, seeds from interploidy crosses develop differently depending on whether the mother or father contributes more chromosome sets, suggesting that maternal and paternal genomes are not functionally equivalent. Here we present the first cytological investigation of seed development following interploidy crosses in Arabidopsis thaliana. We find that crosses between diploid and tetraploid plants in either direction, resulting in double the normal dose of maternal or paternal genomes in the seed, produce viable seeds containing triploid embryos. However, development of the seed and in particular the endosperm is abnormal, with maternal and paternal genomic excess producing complementary phenotypes. A double dose of maternal genomes with respect to paternal contribution inhibits endosperm development and ultimately produces a smaller embryo. In contrast, a double dose of paternal genomes promotes growth of the endosperm and embryo. Reciprocal crosses between diploids and hexaploids, resulting in a triple dose of maternal or paternal genomes, produce seeds that begin development with similar but more extreme phenotypes than those with a double dose, but these invariably abort. One explanation of our observations is that seeds with maternal or paternal excess contain different doses of maternally or paternally expressed imprinted loci affecting endosperm development.

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Philip Wolff ◽  
Hua Jiang ◽  
Guifeng Wang ◽  
Juan Santos-González ◽  
Claudia Köhler

Genomic imprinting is an epigenetic phenomenon causing parent-of-origin specific differential expression of maternally and paternally inherited alleles. While many imprinted genes have been identified in plants, the functional roles of most of them are unknown. In this study, we systematically examine the functional requirement of paternally expressed imprinted genes (PEGs) during seed development in Arabidopsis thaliana. While none of the 15 analyzed peg mutants has qualitative or quantitative abnormalities of seed development, we identify three PEGs that establish postzygotic hybridization barriers in the endosperm, revealing that PEGs have a major role as speciation genes in plants. Our work reveals that a subset of PEGs maintains functional roles in the inbreeding plant Arabidopsis that become evident upon deregulated expression.


2000 ◽  
Vol 12 (12) ◽  
pp. 2367-2381 ◽  
Author(s):  
Ramin Yadegari ◽  
Tetsu Kinoshita ◽  
Ofra Lotan ◽  
Gal Cohen ◽  
Anat Katz ◽  
...  

Planta ◽  
2007 ◽  
Vol 226 (4) ◽  
pp. 805-813 ◽  
Author(s):  
Roberto Schmidt ◽  
Harald Stransky ◽  
Wolfgang Koch

2021 ◽  
Author(s):  
Sichul Lee ◽  
Joohyun Lee ◽  
Felipe K. Ricachenevsky ◽  
Tracy Punshon ◽  
Ryan Tappero ◽  
...  

2020 ◽  
Vol 71 (18) ◽  
pp. 5495-5505 ◽  
Author(s):  
Rui Liu ◽  
Shi-Kai Cao ◽  
Aqib Sayyed ◽  
Huan-Huan Yang ◽  
Jiao Zhao ◽  
...  

Abstract C-to-U RNA editing in plant mitochondria requires the participation of many nucleus-encoded factors, most of which are pentatricopeptide repeat (PPR) proteins. There is a large number of PPR proteins and the functions many of them are unknown. Here, we report a mitochondrion-localized DYW-subgroup PPR protein, PPR27, which functions in the editing of multiple mitochondrial transcripts in maize. The ppr27 mutant is completely deficient in C-to-U editing at the ccmFN-1357 and rps3-707 sites, and editing at six other sites is substantially reduced. The lack of editing at ccmFN-1357 causes a deficiency of CcmFN protein. As CcmFN functions in the maturation pathway of cytochrome proteins that are subunits of mitochondrial complex III, its deficiency results in an absence of cytochrome c1 and cytochrome c proteins. Consequently, the assembly of mitochondrial complex III and super-complex I+III2 is decreased, which impairs the electron transport chain and respiration, leading to arrests in embryogenesis and endosperm development in ppr27. In addition, PPR27 was found to physically interact with ZmMORF1, which interacts with ZmMORF8, suggesting that these three proteins may facilitate C-to-U RNA editing via the formation of a complex in maize mitochondria. This RNA editing is essential for complex III assembly and seed development in maize.


PLoS ONE ◽  
2011 ◽  
Vol 6 (8) ◽  
pp. e23687 ◽  
Author(s):  
Mary Gehring ◽  
Victor Missirian ◽  
Steven Henikoff

Plants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 705 ◽  
Author(s):  
Angel J. Matilla

The production of viable seeds is a key event in the life cycle of higher plants. Historically, abscisic acid (ABA) and gibberellin (GAs) were considered the main hormones that regulate seed formation. However, auxin has recently emerged as an essential player that modulates, in conjunction with ABA, different cellular processes involved in seed development as well as the induction, regulation and maintenance of primary dormancy (PD). This review examines and discusses the key role of auxin as a signaling molecule that coordinates seed life. The cellular machinery involved in the synthesis and transport of auxin, as well as their cellular and tissue compartmentalization, is crucial for the development of the endosperm and seed-coat. Thus, auxin is an essential compound involved in integuments development, and its transport from endosperm is regulated by AGAMOUS-LIKE62 (AGL62) whose transcript is specifically expressed in the endosperm. In addition, recent biochemical and genetic evidence supports the involvement of auxins in PD. In this process, the participation of the transcriptional regulator ABA INSENSITIVE3 (ABI3) is critical, revealing a cross-talk between auxin and ABA signaling. Future experimental aimed at advancing knowledge of the role of auxins in seed development and PD are also discussed.


2019 ◽  
Vol 10 ◽  
Author(s):  
Vicente Balanzà ◽  
Irene Martínez-Fernández ◽  
Shusei Sato ◽  
Martin F. Yanofsky ◽  
Cristina Ferrándiz

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