Genetic analysis of Arabidopsis GATA transcription factor gene family reveals a nitrate-inducible member important for chlorophyll synthesis and glucose sensitivity

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Abstract

The Arabidopsis GATA transcription factor family has 30 members, the biological function of most of which is poorly understood. Homozygous T-DNA insertion lines for 23 of the 30 members were identified and analyzed. Genetic screening of the insertion lines in defined growth conditions revealed one line with an altered phenotype, while the other lines showed no obvious change. This line, SALK_001778, has a T-DNA insertion in the second exon of At5g56860 which prevents the expression of the GATA domain. Genetic analysis of the mutant demonstrated that the phenotypic change is caused by a single gene effect and is recessive to the wild-type allele. In wild-type plants, the expression of At5g56860 is shoot-specific, occurs at an early stage of development and is inducible by nitrate. Loss of expression of At5g56860 in the loss-of-function mutant plants resulted in reduced chlorophyll levels. A transcript profiling experiment revealed that a considerable proportion of genes downregulated in the loss-of-function mutants are involved in carbon metabolism and At5g56860 is thus designated GNC (GATA, nitrate-inducible, carbon metabolism-involved). gnc mutants with no GNC expression are more sensitive to exogenous glucose, and two hexose transporter genes, with a possible connection to glucose signaling, are significantly downregulated, while GNC over-expressing transgenic plants upregulate their expression and are less sensitive to exogenous glucose. These observations suggest a function for GNC in regulating carbon and nitrogen metabolism. © 2005 Blackwell Publishing Ltd.

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Bi, Y. M., Zhang, Y., Signorelli, T., Zhao, R., Zhu, T., & Rothstein, S. (2005). Genetic analysis of Arabidopsis GATA transcription factor gene family reveals a nitrate-inducible member important for chlorophyll synthesis and glucose sensitivity. Plant Journal, 44(4), 680–692. https://doi.org/10.1111/j.1365-313X.2005.02568.x

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