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A Clade-Specific Arabidopsis Gene Connects Primary Metabolism and Senescence.

Jones DC, Zheng W, Huang S, Du C, Zhao X, Yennamalli RM, Sen TZ, Nettleton D, Wurtele ES, Li L - Front Plant Sci (2016)

Bottom Line: In contrast, under experimentally induced senescence, SAQR expression increases in vasculature of cotyledons but not in true leaves.In SAQR KO line, the transcript level of the dirigent-like disease resistance gene (AT1G22900) is increased, while that of the Early Light Induced Protein 1 gene (ELIP1, AT3G22840) is decreased.Taken together, these data indicate that SAQR may function in the QQS network, playing a role in integration of primary metabolism with adaptation to internal and environmental changes, specifically those that affect the process of senescence.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Development and Cell Biology, Iowa State University, Ames IA, USA.

ABSTRACT
Nearly immobile, plants have evolved new components to be able to respond to changing environments. One example is Qua Quine Starch (QQS, AT3G30720), an Arabidopsis thaliana-specific orphan gene that integrates primary metabolism with adaptation to environment changes. SAQR (Senescence-Associated and QQS-Related, AT1G64360), is unique to a clade within the family Brassicaceae; as such, the gene may have arisen about 20 million years ago. SAQR is up-regulated in QQS RNAi mutant and in the apx1 mutant under light-induced oxidative stress. SAQR plays a role in carbon allocation: overexpression lines of SAQR have significantly decreased starch content; conversely, in a saqr T-DNA knockout (KO) line, starch accumulation is increased. Meta-analysis of public microarray data indicates that SAQR expression is correlated with expression of a subset of genes involved in senescence, defense, and stress responses. SAQR promoter::GUS expression analysis reveals that SAQR expression increases after leaf expansion and photosynthetic capacity have peaked, just prior to visible natural senescence. SAQR is expressed predominantly within leaf and cotyledon vasculature, increasing in intensity as natural senescence continues, and then decreasing prior to death. In contrast, under experimentally induced senescence, SAQR expression increases in vasculature of cotyledons but not in true leaves. In SAQR KO line, the transcript level of the dirigent-like disease resistance gene (AT1G22900) is increased, while that of the Early Light Induced Protein 1 gene (ELIP1, AT3G22840) is decreased. Taken together, these data indicate that SAQR may function in the QQS network, playing a role in integration of primary metabolism with adaptation to internal and environmental changes, specifically those that affect the process of senescence.

No MeSH data available.


Related in: MedlinePlus

Model of SAQR function. Decreased QQS expression or increased stress cause greater starch accumulation. SAQR expression is up-regulated by multiple stresses and down-regulated by QQS (Li et al., 2015b), JA, and CK (data of Figure 4). Multiple stresses increase starch accumulation; QQS, MeJA (Babst et al., 2005) and CK decrease starch accumulation. SAQR expression increases starch accumulation. Our working model is that SAQR mediates changes in starch accumulation. SAQR expression also decreases time to flowering under short day conditions. This change in flowering time may occur via some aspect of starch metabolism, or by a mechanism independent of starch metabolism. Green arrows, promotes; red blocked lines, represses.
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Figure 7: Model of SAQR function. Decreased QQS expression or increased stress cause greater starch accumulation. SAQR expression is up-regulated by multiple stresses and down-regulated by QQS (Li et al., 2015b), JA, and CK (data of Figure 4). Multiple stresses increase starch accumulation; QQS, MeJA (Babst et al., 2005) and CK decrease starch accumulation. SAQR expression increases starch accumulation. Our working model is that SAQR mediates changes in starch accumulation. SAQR expression also decreases time to flowering under short day conditions. This change in flowering time may occur via some aspect of starch metabolism, or by a mechanism independent of starch metabolism. Green arrows, promotes; red blocked lines, represses.

Mentions: Although the molecular function of SAQR is unclear, there are several indications of its potential biological functions (Figure 7). Reflecting the patterns of senescence itself, during natural senescence, SAQR is up-regulated in the cotyledons and true leaves, whereas in light stress-induced senescence, SAQR expression is up-regulated only in the cotyledons, and is repressed in the true leaves. This is evidenced not only in the SAQR expression patterns, but also by the tight correlation of expression of many SAG genes to SAQR. Several factors might lead to this distinction between SAQR expression in true leaves and cotyledons. Cotyledon senescence is less understood than leaf senescence, but the processes have developmental and molecular differences (Du et al., 2014). Cotyledon senescence is induced by different signals than is true leaf senescence; it has been suggested that these differences are due to the cotyledon’s early function as a storage organ (Weaver and Amasino, 2001). Some sets of genes are differentially expressed in cotyledons compared to true leaves; many of the genes specific to or differentially expressed in soybean cotyledons are involved in early mobilization of nutrients, indicating a rapid transfer of resources to the seedling (Brown and Hudson, 2015). This mimics the nutrient transfer process that occurs under senescence of older leaves (Diaz et al., 2008). In fact, when plant are treated by light after dark, naturally senescing true leaves that are already undergoing transfer of nutrients to the rest of the plant exhibit less delay in senescence compared to younger leaves (Weaver and Amasino, 2001). The increase of SAQR expression in cotyledons under light stress likely reflects this difference between cotyledons and early true leaves.


A Clade-Specific Arabidopsis Gene Connects Primary Metabolism and Senescence.

Jones DC, Zheng W, Huang S, Du C, Zhao X, Yennamalli RM, Sen TZ, Nettleton D, Wurtele ES, Li L - Front Plant Sci (2016)

Model of SAQR function. Decreased QQS expression or increased stress cause greater starch accumulation. SAQR expression is up-regulated by multiple stresses and down-regulated by QQS (Li et al., 2015b), JA, and CK (data of Figure 4). Multiple stresses increase starch accumulation; QQS, MeJA (Babst et al., 2005) and CK decrease starch accumulation. SAQR expression increases starch accumulation. Our working model is that SAQR mediates changes in starch accumulation. SAQR expression also decreases time to flowering under short day conditions. This change in flowering time may occur via some aspect of starch metabolism, or by a mechanism independent of starch metabolism. Green arrows, promotes; red blocked lines, represses.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940393&req=5

Figure 7: Model of SAQR function. Decreased QQS expression or increased stress cause greater starch accumulation. SAQR expression is up-regulated by multiple stresses and down-regulated by QQS (Li et al., 2015b), JA, and CK (data of Figure 4). Multiple stresses increase starch accumulation; QQS, MeJA (Babst et al., 2005) and CK decrease starch accumulation. SAQR expression increases starch accumulation. Our working model is that SAQR mediates changes in starch accumulation. SAQR expression also decreases time to flowering under short day conditions. This change in flowering time may occur via some aspect of starch metabolism, or by a mechanism independent of starch metabolism. Green arrows, promotes; red blocked lines, represses.
Mentions: Although the molecular function of SAQR is unclear, there are several indications of its potential biological functions (Figure 7). Reflecting the patterns of senescence itself, during natural senescence, SAQR is up-regulated in the cotyledons and true leaves, whereas in light stress-induced senescence, SAQR expression is up-regulated only in the cotyledons, and is repressed in the true leaves. This is evidenced not only in the SAQR expression patterns, but also by the tight correlation of expression of many SAG genes to SAQR. Several factors might lead to this distinction between SAQR expression in true leaves and cotyledons. Cotyledon senescence is less understood than leaf senescence, but the processes have developmental and molecular differences (Du et al., 2014). Cotyledon senescence is induced by different signals than is true leaf senescence; it has been suggested that these differences are due to the cotyledon’s early function as a storage organ (Weaver and Amasino, 2001). Some sets of genes are differentially expressed in cotyledons compared to true leaves; many of the genes specific to or differentially expressed in soybean cotyledons are involved in early mobilization of nutrients, indicating a rapid transfer of resources to the seedling (Brown and Hudson, 2015). This mimics the nutrient transfer process that occurs under senescence of older leaves (Diaz et al., 2008). In fact, when plant are treated by light after dark, naturally senescing true leaves that are already undergoing transfer of nutrients to the rest of the plant exhibit less delay in senescence compared to younger leaves (Weaver and Amasino, 2001). The increase of SAQR expression in cotyledons under light stress likely reflects this difference between cotyledons and early true leaves.

Bottom Line: In contrast, under experimentally induced senescence, SAQR expression increases in vasculature of cotyledons but not in true leaves.In SAQR KO line, the transcript level of the dirigent-like disease resistance gene (AT1G22900) is increased, while that of the Early Light Induced Protein 1 gene (ELIP1, AT3G22840) is decreased.Taken together, these data indicate that SAQR may function in the QQS network, playing a role in integration of primary metabolism with adaptation to internal and environmental changes, specifically those that affect the process of senescence.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Development and Cell Biology, Iowa State University, Ames IA, USA.

ABSTRACT
Nearly immobile, plants have evolved new components to be able to respond to changing environments. One example is Qua Quine Starch (QQS, AT3G30720), an Arabidopsis thaliana-specific orphan gene that integrates primary metabolism with adaptation to environment changes. SAQR (Senescence-Associated and QQS-Related, AT1G64360), is unique to a clade within the family Brassicaceae; as such, the gene may have arisen about 20 million years ago. SAQR is up-regulated in QQS RNAi mutant and in the apx1 mutant under light-induced oxidative stress. SAQR plays a role in carbon allocation: overexpression lines of SAQR have significantly decreased starch content; conversely, in a saqr T-DNA knockout (KO) line, starch accumulation is increased. Meta-analysis of public microarray data indicates that SAQR expression is correlated with expression of a subset of genes involved in senescence, defense, and stress responses. SAQR promoter::GUS expression analysis reveals that SAQR expression increases after leaf expansion and photosynthetic capacity have peaked, just prior to visible natural senescence. SAQR is expressed predominantly within leaf and cotyledon vasculature, increasing in intensity as natural senescence continues, and then decreasing prior to death. In contrast, under experimentally induced senescence, SAQR expression increases in vasculature of cotyledons but not in true leaves. In SAQR KO line, the transcript level of the dirigent-like disease resistance gene (AT1G22900) is increased, while that of the Early Light Induced Protein 1 gene (ELIP1, AT3G22840) is decreased. Taken together, these data indicate that SAQR may function in the QQS network, playing a role in integration of primary metabolism with adaptation to internal and environmental changes, specifically those that affect the process of senescence.

No MeSH data available.


Related in: MedlinePlus