The maize heterotrimeric G protein ß subunit controls shoot meristem development and immune responses.
Proc Natl Acad Sci U S A
; 117(3): 1799-1805, 2020 01 21.
Article
em En
| MEDLINE
| ID: mdl-31852823
Heterotrimeric G proteins are important transducers of receptor signaling, functioning in plants with CLAVATA receptors in controlling shoot meristem size and with pathogen-associated molecular pattern receptors in basal immunity. However, whether specific members of the heterotrimeric complex potentiate cross-talk between development and defense, and the extent to which these functions are conserved across species, have not yet been addressed. Here we used CRISPR/Cas9 to knock out the maize G protein ß subunit gene (Gß) and found that the mutants are lethal, differing from those in Arabidopsis, in which homologous mutants have normal growth and fertility. We show that lethality is caused not by a specific developmental arrest, but by autoimmunity. We used a genetic diversity screen to suppress the lethal Gß phenotype and also identified a maize Gß allele with weak autoimmune responses but strong development phenotypes. Using these tools, we show that Gß controls meristem size in maize, acting epistatically with G protein α subunit gene (Gα), suggesting that Gß and Gα function in a common signaling complex. Furthermore, we used an association study to show that natural variation in Gß influences maize kernel row number, an important agronomic trait. Our results demonstrate the dual role of Gß in immunity and development in a cereal crop and suggest that it functions in cross-talk between these competing signaling networks. Therefore, modification of Gß has the potential to optimize the trade-off between growth and defense signaling to improve agronomic production.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Brotos de Planta
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Meristema
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Zea mays
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Subunidades beta da Proteína de Ligação ao GTP
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Imunidade Vegetal
Idioma:
En
Revista:
Proc Natl Acad Sci U S A
Ano de publicação:
2020
Tipo de documento:
Article