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Mutations in HISTONE ACETYLTRANSFERASE1 affect sugar response and gene expression in Arabidopsis.

Heisel TJ, Li CY, Grey KM, Gibson SI - Front Plant Sci (2013)

Bottom Line: Histone acetyltransferases increase transcription of specific genes by acetylating histones associated with those genes.SnRK1 complexes have been shown to function as central regulators of plant nutrient and energy status.Involvement of a histone acetyltransferase in sugar response provides a possible mechanism whereby nutritional status could exert long-term effects on plant development and metabolism.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota Saint Paul, MN, USA.

ABSTRACT
Nutrient response networks are likely to have been among the first response networks to evolve, as the ability to sense and respond to the levels of available nutrients is critical for all organisms. Although several forward genetic screens have been successful in identifying components of plant sugar-response networks, many components remain to be identified. Toward this end, a reverse genetic screen was conducted in Arabidopsis thaliana to identify additional components of sugar-response networks. This screen was based on the rationale that some of the genes involved in sugar-response networks are likely to be themselves sugar regulated at the steady-state mRNA level and to encode proteins with activities commonly associated with response networks. This rationale was validated by the identification of hac1 mutants that are defective in sugar response. HAC1 encodes a histone acetyltransferase. Histone acetyltransferases increase transcription of specific genes by acetylating histones associated with those genes. Mutations in HAC1 also cause reduced fertility, a moderate degree of resistance to paclobutrazol and altered transcript levels of specific genes. Previous research has shown that hac1 mutants exhibit delayed flowering. The sugar-response and fertility defects of hac1 mutants may be partially explained by decreased expression of AtPV42a and AtPV42b, which are putative components of plant SnRK1 complexes. SnRK1 complexes have been shown to function as central regulators of plant nutrient and energy status. Involvement of a histone acetyltransferase in sugar response provides a possible mechanism whereby nutritional status could exert long-term effects on plant development and metabolism.

No MeSH data available.


Related in: MedlinePlus

The hac1 mutants are moderately resistant to the inhibitory effects of paclobutrazol on seed germination. Mutant and wild-type Col-0 (WT) seeds were surface sterilized, imbibed in the dark at 4°C for 3 days and then sown on Petri plates with Arabidopsis minimal media and 0 or 34 μM paclobutrazol. The Petri plates were incubated under continuous light at 22°C and scored for seed germination at regular intervals. The spy-3 mutant (Jacobsen and Olszewski, 1993) was included as a positive control. Error bars indicate standard deviations. N = 2.
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Figure 4: The hac1 mutants are moderately resistant to the inhibitory effects of paclobutrazol on seed germination. Mutant and wild-type Col-0 (WT) seeds were surface sterilized, imbibed in the dark at 4°C for 3 days and then sown on Petri plates with Arabidopsis minimal media and 0 or 34 μM paclobutrazol. The Petri plates were incubated under continuous light at 22°C and scored for seed germination at regular intervals. The spy-3 mutant (Jacobsen and Olszewski, 1993) was included as a positive control. Error bars indicate standard deviations. N = 2.

Mentions: Mutations that lead to sugar-insensitive or hypersensitive phenotypes often also affect phytohormone response. For example, a number of sugar-insensitive mutants have been found to be resistant to the inhibitory effects of abscisic acid and/or paclobutrazol (an inhibitor of the biosynthesis of gibberellins) on seed germination (Arenas-Huertero et al., 2000; Huijser et al., 2000; Laby et al., 2000; Gibson et al., 2001; Rook et al., 2001; Huang et al., 2008). Therefore, hac1 mutants were tested for altered sensitivity to the inhibitory effects of paclobutrazol on seed germination. All three of the hac1 mutants tested exhibited slightly faster rates of seed germination on media supplemented with 34 μM paclobutrazol than did seeds from wild-type plants (Figure 4). In addition, the percentages of seeds that germinated within 8 days on 34 μM paclobutrazol were significantly higher for each of the three hac1 mutant lines tested than for the wild-type line. Comparison of the percentages of hac1 and wild-type seeds that had germinated within 8 days on 34 μM paclobutrazol showed that these percentages differed with p values of 0.02, 0.0002, and 0.06 for hac1-2, hac1-3, and hac1-6, respectively. However, the germination rates of the hac1 mutants were much lower on 34 μM paclobutrazol than the germination rates of the spy-3 mutant. The spy-3 mutant was previously identified as a paclobutrazol-resistant mutant (Jacobsen and Olszewski, 1993) and was included in these experiments as a positive control. Thus, the results of these experiments indicate that mutations in HAC1 confer a modest degree of resistance to the inhibitory effects of paclobutrazol on seed germination.


Mutations in HISTONE ACETYLTRANSFERASE1 affect sugar response and gene expression in Arabidopsis.

Heisel TJ, Li CY, Grey KM, Gibson SI - Front Plant Sci (2013)

The hac1 mutants are moderately resistant to the inhibitory effects of paclobutrazol on seed germination. Mutant and wild-type Col-0 (WT) seeds were surface sterilized, imbibed in the dark at 4°C for 3 days and then sown on Petri plates with Arabidopsis minimal media and 0 or 34 μM paclobutrazol. The Petri plates were incubated under continuous light at 22°C and scored for seed germination at regular intervals. The spy-3 mutant (Jacobsen and Olszewski, 1993) was included as a positive control. Error bars indicate standard deviations. N = 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3713338&req=5

Figure 4: The hac1 mutants are moderately resistant to the inhibitory effects of paclobutrazol on seed germination. Mutant and wild-type Col-0 (WT) seeds were surface sterilized, imbibed in the dark at 4°C for 3 days and then sown on Petri plates with Arabidopsis minimal media and 0 or 34 μM paclobutrazol. The Petri plates were incubated under continuous light at 22°C and scored for seed germination at regular intervals. The spy-3 mutant (Jacobsen and Olszewski, 1993) was included as a positive control. Error bars indicate standard deviations. N = 2.
Mentions: Mutations that lead to sugar-insensitive or hypersensitive phenotypes often also affect phytohormone response. For example, a number of sugar-insensitive mutants have been found to be resistant to the inhibitory effects of abscisic acid and/or paclobutrazol (an inhibitor of the biosynthesis of gibberellins) on seed germination (Arenas-Huertero et al., 2000; Huijser et al., 2000; Laby et al., 2000; Gibson et al., 2001; Rook et al., 2001; Huang et al., 2008). Therefore, hac1 mutants were tested for altered sensitivity to the inhibitory effects of paclobutrazol on seed germination. All three of the hac1 mutants tested exhibited slightly faster rates of seed germination on media supplemented with 34 μM paclobutrazol than did seeds from wild-type plants (Figure 4). In addition, the percentages of seeds that germinated within 8 days on 34 μM paclobutrazol were significantly higher for each of the three hac1 mutant lines tested than for the wild-type line. Comparison of the percentages of hac1 and wild-type seeds that had germinated within 8 days on 34 μM paclobutrazol showed that these percentages differed with p values of 0.02, 0.0002, and 0.06 for hac1-2, hac1-3, and hac1-6, respectively. However, the germination rates of the hac1 mutants were much lower on 34 μM paclobutrazol than the germination rates of the spy-3 mutant. The spy-3 mutant was previously identified as a paclobutrazol-resistant mutant (Jacobsen and Olszewski, 1993) and was included in these experiments as a positive control. Thus, the results of these experiments indicate that mutations in HAC1 confer a modest degree of resistance to the inhibitory effects of paclobutrazol on seed germination.

Bottom Line: Histone acetyltransferases increase transcription of specific genes by acetylating histones associated with those genes.SnRK1 complexes have been shown to function as central regulators of plant nutrient and energy status.Involvement of a histone acetyltransferase in sugar response provides a possible mechanism whereby nutritional status could exert long-term effects on plant development and metabolism.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota Saint Paul, MN, USA.

ABSTRACT
Nutrient response networks are likely to have been among the first response networks to evolve, as the ability to sense and respond to the levels of available nutrients is critical for all organisms. Although several forward genetic screens have been successful in identifying components of plant sugar-response networks, many components remain to be identified. Toward this end, a reverse genetic screen was conducted in Arabidopsis thaliana to identify additional components of sugar-response networks. This screen was based on the rationale that some of the genes involved in sugar-response networks are likely to be themselves sugar regulated at the steady-state mRNA level and to encode proteins with activities commonly associated with response networks. This rationale was validated by the identification of hac1 mutants that are defective in sugar response. HAC1 encodes a histone acetyltransferase. Histone acetyltransferases increase transcription of specific genes by acetylating histones associated with those genes. Mutations in HAC1 also cause reduced fertility, a moderate degree of resistance to paclobutrazol and altered transcript levels of specific genes. Previous research has shown that hac1 mutants exhibit delayed flowering. The sugar-response and fertility defects of hac1 mutants may be partially explained by decreased expression of AtPV42a and AtPV42b, which are putative components of plant SnRK1 complexes. SnRK1 complexes have been shown to function as central regulators of plant nutrient and energy status. Involvement of a histone acetyltransferase in sugar response provides a possible mechanism whereby nutritional status could exert long-term effects on plant development and metabolism.

No MeSH data available.


Related in: MedlinePlus