Ped3p is a Peroxisomal ATP-Binding Cassette Transporter that might Supply Substrates for Fatty Acid β-Oxidation

Hayashi, Makoto; Nito, Kazumasa; Takei-Hoshi, Rie; Yagi, Mina; Kondo, Maki; Suenaga, A.; Yamaya, Tomoyuki; Nishimura, Mikio

doi:10.1093/pcp/pcf023

Cited by 179 publications

(222 citation statements)

References 33 publications

(41 reference statements)

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“…Seedling establishment phenotypes can be frequently rescued by the provision of a carbon supply. 32 To elucidate this point we have analyzed wild type and Atltp3 lines for seedling growth in darkness but in the presence of 1% sucrose (Fig. 3 A-B).…”

Section: Resultsmentioning

confidence: 99%

“…This behavior is similar to that exhibited by Arabidopsis mutants disrupted in lipid mobilization such as Ped3p. 32 Accumulated evidence indicates that several mutants in oil mobilization pathways are compromised in seedling establishment [33][34] since the most important function of fatty acid b-oxidation is to support postgerminative growth. 35 In order to verify if the phenotype observed in Atltp3 correlates with the inability to use seed oil reserves we have first analyzed the fatty acid profile of mutant and wild type seeds just before germination was triggered.…”

Section: Resultsmentioning

confidence: 99%

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On the role of a Lipid-Transfer Protein. Arabidopsis ltp3 mutant is compromised in germination and seedling growth.

Pagnussat

Oyarburo

Cimmino³

et al. 2015

Plant Signaling & Behavior

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

On the role of a Lipid-Transfer Protein. Arabidopsis ltp3 mutant is compromised in germination and seedling growth.

Pagnussat

Oyarburo

Cimmino³

et al. 2015

Plant Signaling & Behavior

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“…Blocking several steps of peroxisomal b-oxidation simultaneously by a mutation in the gene encoding the multifunctional protein AIM1 causes twisted leaves, abnormal inflorescence meristems, and a severe reduction of fertility (Richmond and Bleecker, 1999). Similar phenotypes are found in the ped1ped3 double mutant, where acyl-CoA import and its subsequent cleavage in peroxisomes are both impaired (Hayashi et al, 2002). Moreover, combination of loss-of-function mutations in the peroxisomal medium-and short-chain acyl-CoA oxidase genes leads to early embryo lethality (Rylott et al, 2003).…”

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confidence: 79%

The Peroxisome Deficient Arabidopsis Mutant sse1 Exhibits Impaired Fatty Acid Synthesis

2004

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The Arabidopsis Shrunken Seed 1 (SSE1) gene encodes a homolog of the peroxisome biogenesis factor Pex16p, and a loss-of-function mutation in this gene alters seed storage composition. Two lines of evidence support a function for SSE1 in peroxisome biogenesis: the peroxisomal localization of a green fluorescent protein-SSE1 fusion protein and the lack of normal peroxisomes in sse1 mutant embryos. The green fluorescent protein-SSE1 colocalizes with the red fluorescent protein (RFP)-labeled peroxisomal markers RFP-peroxisome targeting signal 1 and peroxisome targeting signal 2-RFP in transgenic Arabidopsis. Each peroxisomal marker exhibits a normal punctate peroxisomal distribution in the wild type but not the sse1 mutant embryos. Further studies reported here were designed toward understanding carbon metabolism in the sse1 mutant. A time course study of dissected embryos revealed a dramatic rate decrease in oil accumulation and an increase in starch accumulation. Introduction of starch synthesis mutations into the sse1 background did not restore oil biosynthesis. This finding demonstrated that reduction in oil content in sse1 is not caused by increased carbon flow to starch. To identify the blocked steps in the sse1 oil deposition pathway, developing sse1 seeds were supplied radiolabeled oil synthesis precursors. The ability of sse1 to incorporate oleic acid, but not pyruvate or acetate, into triacylglycerol indicated a defect in the fatty acid biosynthetic pathway in this mutant. Taken together, the results point to a possible role for peroxisomes in the net synthesis of fatty acids in addition to their established function in lipid catabolism. Other possible interpretations of the results are discussed.

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“…cts-1 mutant seeds cannot germinate in the absence of classical dormancybreaking treatments and do not establish in the absence of an exogenous energy source because of their inability to mobilize storage lipids by b-oxidation (Footitt et al, 2002(Footitt et al, , 2006. Mutant cts alleles have also been identified in screens for seedlings resistant to 2,4-dichlorophenoxybutyric acid and indole butyric acid (IBA; Zolman et al, 2001;Hayashi et al, 2002). These compounds are converted by one round of b-oxidation to the bioactive auxins, 2,4-dichlorophenoxyacetic acid and indole acetic acid (IAA), respectively, which stunt roots.…”

mentioning

confidence: 99%

“…It is probable that the low residual levels of JA in cts mutants are sufficient for fertility because McConn and Browse (1996) used a triple fatty acid desaturase mutant with a leaky fad7 allele to demonstrate the existence of a threshold limit for the JA precursor, linolenic acid (18:3), and by extension, JA itself, for male fertility. Intriguingly, it has been reported that the doublemutant ped1,ped3-1, which lacks both CTS and KAT2, is sterile (Hayashi et al, 2002), perhaps because the compound effect of mutating both genes reduces JA levels below the fertility threshold. The apparently ubiquitous expression of CTS and the known role of JA in male fertility led us to examine in more detail the roles of this transporter during postgerminative growth to determine what impact loss of CTS function has on vegetative and reproductive processes.…”

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confidence: 99%

The COMATOSE ATP-Binding Cassette Transporter Is Required for Full Fertility in Arabidopsis

et al. 2007

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COMATOSE (CTS) encodes a peroxisomal ATP-binding cassette transporter required not only for b-oxidation of storage lipids during germination and establishment, but also for biosynthesis of jasmonic acid and conversion of indole butyric acid to indole acetic acid. cts mutants exhibited reduced fertilization, which was rescued by genetic complementation, but not by exogenous application of jasmonic acid or indole acetic acid. Reduced fertilization was also observed in thiolase (kat2-1) and peroxisomal acyl-Coenzyme A synthetase mutants (lacs6-1,lacs7-1), indicating a general role for b-oxidation in fertility. Genetic analysis revealed reduced male transmission of cts alleles and both cts pollen germination and tube growth in vitro were impaired in the absence of an exogenous carbon source. Aniline blue staining of pollinated pistils demonstrated that pollen tube growth was affected only when both parents bore the cts mutation, indicating that expression of CTS in either male or female tissues was sufficient to support pollen tube growth in vivo. Accordingly, abundant peroxisomes were detected in a range of maternal tissues. Although g-aminobutyric acid levels were reduced in flowers of cts mutants, they were unchanged in kat2-1, suggesting that alterations in g-aminobutyric acid catabolism do not contribute to the reduced fertility phenotype through altered pollen tube targeting. Taken together, our data support an important role for b-oxidation in fertility in Arabidopsis (Arabidopsis thaliana) and suggest that this pathway could play a role in the mobilization of lipids in both pollen and female tissues.

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Ped3p is a Peroxisomal ATP-Binding Cassette Transporter that might Supply Substrates for Fatty Acid β-Oxidation

Cited by 179 publications

References 33 publications

On the role of a Lipid-Transfer Protein. Arabidopsis ltp3 mutant is compromised in germination and seedling growth.

On the role of a Lipid-Transfer Protein. Arabidopsis ltp3 mutant is compromised in germination and seedling growth.

The Peroxisome Deficient Arabidopsis Mutant sse1 Exhibits Impaired Fatty Acid Synthesis

The COMATOSE ATP-Binding Cassette Transporter Is Required for Full Fertility in Arabidopsis

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