- Email: [email protected]
Plant development: A role for sterols in embryogenesis
Dispatch
R601
Plant development: A role for sterols in embryogenesis Steven D. Clouse
The Arabidopsis mutants fackel and sterol methyltransferase 1 have defects associated with body organization of the seedling. Molecular analysis of these mutants has revealed that plant sterols may be key signaling molecules influencing position-dependent cell fate during embryonic development. Address: Department of Horticultural Science, North Carolina State University, Raleigh, North Carolina 27695-7609, USA. Current Biology 2000, 10:R601–R604 0960-9822/00/$ – see front matter © 2000 Elsevier Science Ltd. All rights reserved.
Sterols are isoprenoid-derived compounds that play essential roles in the development of all eukaryotic organisms. Bulk sterols, such as cholesterol in animals, ergosterol in yeast and sitosterol and campesterol in plants, are integral membrane components which serve to regulate the fluidity and permeability of membranes and directly affect the activity of membrane associated proteins, including enzymes and signal transduction components [1]. These same sterols also serve as biosynthetic precursors of steroid hormones, including mammalian androgens, estrogens and glucocorticoids; insect ecdysteroids; fungal antheridiol and oogoniol; and plant brassinosteroids. Moreover, recent evidence from animal studies suggests that, in addition to the well-known mechanism of steroid hormone action, sterols can themselves serve as ligands for nuclear receptors and interact with other transcription complexes to directly modulate signal transduction pathways [2]. Given the multiple and critical roles that sterols play, it is not surprising that mutations in genes encoding sterol biosynthetic enzymes can have a dramatic affect on eukaryotic development. Four plant mutants with lesions in the sterol biosynthetic pathway have now been identified, in addition to five mutants known to have defects in the specific pathway leading to brassinosteroids. Comparison of the phenotypes of these mutants and their responses to brassinosteroid application is revealing an intriguing story about the roles that sterols and their hormone derivatives play in controlling both embryonic and post-embryonic plant development. The critical importance of brassinosteroids in plant growth and development became apparent in recent years as a result of combined molecular genetic and biochemical analyses [3]. Brassinolide, the most active brassinosteroid, is derived from campesterol via a series of sidechain hydroxylations combined with ring reductions, oxidations and epimerizations. Mutants affected in several steps of
this pathway have been identified, including constitutive photomorphogenesis and dwarfism (cpd ), dwarf4 (dwf4) and de-etiolated2 (det2). These mutants show a characteristic phenotype in the light, including dwarf stature, dark green and rounded leaves, prolonged life-span, reduced fertility and altered vascular development. In the dark, they exhibit features of light-grown plants, including shortened hypocotyl and open cotyledons [4]. All of these phenotypic alterations can be rescued by exogenous application of brassinolide. Mutants with defects in the sterol biosynthetic pathway preceding campesterol have also been identified. A screen of ethyl-methanesulfonate-mutagenized Arabidopsis seedlings by gas chromatography uncovered a mutant, ste1 [5], that accumulated ∆7 sterols with a decrease in the corresponding ∆5 sterols. Transgenic plants expressing the yeast ERG3 gene, which encodes a ∆7-C-5-desaturase, regained the normal sterol profile. The ste1 mutant first identified apparently carried a weak or leaky allele, as it showed no visible phenotype. A null allele of ste1, dwarf7 (dwf7) was discovered in a screen for dwarfs in a population of T-DNA-mutagenized Arabidopsis plants. This mutant had many of the phenotypic features of brassinosteroiddeficient mutants (although not as severe), which could be rescued to wild-type by brassinosteroid treatment [6]. Feeding experiments with labeled intermediates showed that the dwf7 mutant accumulated episterol, while 5-dehydroepisterol was not detected. This, coupled with significant sequence similarity of the DWF7 gene product to yeast C-5 desaturases, showed that the dwf7/ste1 lesions occur in the gene encoding ∆7-C-5desaturase. Similar types of analysis showed that the allelic mutants dwarf1/dimunito/cabbage1 (dwf1/dim/cbb1) are defective in the conversion of 24-methylenecholesterol to campesterol (reviewed in [4]). These mutants share many of the phenotypic characteristics of dwf7, including intermediate dwarfism and rescue to wild-type by brassinosteroid treatment. Three recent papers [7–9] have identified mutants with blocks very early in the sterol biosynthetic pathway that have some of the characteristics of brassinosteroiddeficient mutants as adult plants, but show unique defects during embryogenesis not previously seen in brassinosteroid mutants or sterol biosynthetic mutants affected later in the pathway. Moreover, these mutants are not rescued by brassinosteroid treatment. The fackel mutant of Arabidopsis was initially identified in a systematic screen for mutations affecting body organization in
R602
Current Biology Vol 10 No 16
Arabidopsis seedlings [10]. The extra-long-lifespan mutant was uncovered in a genetic screen for constitutive cytokinin response mutants, and subsequent analysis revealed that extra-long-lifespan is an allele of fackel [7]. Molecular characterization of the fackel mutants by two independent groups has provided strong evidence that the FACKEL gene encodes a sterol C-14 reductase required for the conversion of 4α-methyl-5α-ergosta8,14,24(28)-trien-3β-ol to 4α-methylfecosterol [7,8]. The FACKEL protein shows significant sequence similarity to animal and fungal C-14 sterol reductases, and FACKEL cDNA was found to rescue the defective sterol C-14 reductase in the yeast mutant erg24. Furthermore, the levels of brassinosteroids, campesterol and sitosterol were found to be severely reduced in the mutant, whereas the sterol C-14 reductase substrate had accumulated to ten times its wild-type level. Interestingly, the fackel mutant accumulates three unusual 8,14-diene sterols, as also observed in plant cell suspension cultures treated with 15-azasterol, an inhibitor of sterol C-14 reductase. The sterol methyltransferase 1 (smt1) mutant of Arabidopsis shares many of the phenotypic properties of fackel and has been shown to have a defect in a step very early in the sterol biosynthetic pathway [9]. The SMT1 gene encodes an enzyme capable of C-24 alkylation of the sterol side chain in the presence of S-adenosylmethionine, and recombinant SMT1 protein was found to catalyse the conversion of cycloartenol to 24-methylene cycloartenol. Cholesterol accumulates in the smt1 mutant at the expense of sitosterol, although other sterol levels are relatively normal. During development of the Arabidopsis embryo, cell fate is determined in a position-dependent manner, generating an apical–basal pattern along the main body axis and a series of concentric rings in a radial pattern around the main axis. Several distinct stages of embryogenesis can be distinguished, including globular, heart and torpedo stages. Embryogenesis was found to be severely disrupted in fackel mutants, starting with a lack of asymmetrical cell division in the globular-stage embryo. While wild-type embryos progress to the heart stage, fackel embryos remain globular and disorganized. Multiple shoot apical meristems are initiated in the fackel mutant, and developing seedlings often have more than the normal two cotyledons. The cotyledons appear to be directly attached to the root, with little development of the hypocotyl (Figure 1); root development itself is also altered. In situ hybridization showed that the FACKEL gene is prominently expressed in wild-type plants during embryo development [8]. The smt1 mutant [9] shows similar defects in embryogenesis to the fackel mutant, and the wild-type gene shows similar expression levels. As mentioned above, adult fackel plants exhibit many of the
features of brassinosteroid-deficient mutants — and are themselves brassinosteroid-deficient — but they cannot be rescued by brassinosteroid treatment, even though they retain some sensitivity to brassinosteroids [7]. Why do plants compromised early in the sterol biosynthetic pathway show severe defects in embryogenesis, while those affected later in the pathway, such as dwf7/ste1 and dwf1/dim1, do not? The simple reduction in bulk sterols, such as sitosterol and campesterol, cannot be the only answer, as dwf7 and dwf1 also have reduced sterol levels but do not show the same defects. Furthermore, fackel is not rescued by treatment with high levels of these sterols and smt1 has relatively normal levels of campesterol [9]. One possibility is that the unusual sterols that accumulate in the mutants become incorporated into membranes, altering their properties. Basic cell division is not affected in the fackel mutant, however, as mutant callus cells proliferate and cell-expansion defects in the embryo are not observed until the globular stage, by when about 60 cells have undergone division [8]. This argues against the notion that a general membrane defect disturbs cell division and expansion in these mutants. An intriguing possibility is that a sterol molecule itself serves as a signal that controls pattern formation within the embryo. This sterol could be one of the intermediates in the pathway between the product of the C-14 reductase and the substrate of the ∆7-C-5-desaturase, or these sterols might serve as precursors for as-yet unidentified sterols or nonbrassinosteroid hormones. The unusual sterols accumulated in the mutants could also act as signals, although the fact the fackel and smt1 have similar embryonic phenotypes, but accumulate different sterols, argues against this. A role for non-steroid hormone sterols in signaling has precedence in the animal kingdom. Hedgehog proteins are a family of signaling molecules crucial in early development of invertebrates and vertebrates. Both Drosophila Hedgehog and mouse Sonic hedgehog have been shown to undergo a covalent modification with cholesterol that is essential for proper spatial patterning during embryogenesis. Other examples include the activation of meiosis in mammalian cells by the cholesterol precursors 4,4-dimethyl-5α-cholesta-8,14,24trien-3β-ol and 4,4-dimethyl-5α-cholesta-8,14,24-dien-3βol, and the activation of nuclear receptors by oxysterols such as 25-, 26- and 27-hydroxycholesterol [2]. Brassinosteroids have become well-established signaling molecules required for normal post-embryonic plant development. The molecular analyses of fackel and smt1 mutants have raised the exciting possibility that other compounds of the sterol biosynthetic pathway may play a hormonal-like role in controlling embryogenesis and position-dependent cell fates. The ready availability of
Dispatch
R603
Figure 1 Biosynthetic pathways of sterols and brassinosteroids required for normal plant development. Cycloartenol, a polycyclic sterol intermediate unique to plants, is alkylated at C-24 by sterol methyltransferase 1, and converted to the trien form in a series of steps. The trien is reduced by the FACKEL gene product, a C-14 sterol reductase, to yield 4α-methylfecosterol, which then proceeds via a split pathway to the bulk membrane sterols sitosterol and campesterol in several steps, including a desaturation and C-24 reduction. Campesterol also serves as the progenitor of brassinosteroids, which are required for normal post-embryonic development. Defects in embryogenesis observed in the fackel mutant suggest that a non-brassinosteroid sterol intermediate might serve as a signal for proper pattern formation in the developing embryo. (a) Morphological differences between wild-type (left) and fackel (right) embryos at the heart stage. (b) An adult fackel mutant shows some of the characteristics of brassinosteroid-deficient mutants. (c) The fackel mutant often has multiple cotyledons and no apparent hypocotyl. (d) Several unique dien sterols accumulate in the fackel mutant (with the same ring structure as the C-14 reductase substrate).
Mevalonic acid
(d)
(a)
(b)
HO
5α-Cholesta8,14-dien-3β-ol (24R)-5α-Ergosta8,14,-dien-3β-ol
(c)
(24R)-5α-Stigmasta8,14-dien-3β-ol
Cycloartenol
fackel
C-14 sterol reductase
HO
HO
4α-Methyl-5α-ergosta-8,14,24(28)-trien-3β-ol
4α-Methylfecosterol
Citrostadienol
24-Methylenelophenol
Avenasterol
Episterol
dwf7/ste1 (∆7 Sterol C-5-desaturase)
5-Dehydroavenasterol
5-Dehydroepisterol
Isofucosterol
24-Methylenecholesterol dwf1/dim (C-24 reductase)
HO
HO
HO
Sitosterol
Stigmasterol
det2
Campesterol dwf4 cpd
Membrane sterols Brassinosteroids
Wild type
Current Biology
genetic and biochemical tools make it likely that progress in uncovering these factors will be much more rapid than the seventeen-year span that elapsed between discovery of the structure of brassinolide and the acceptance of brassinosteroids as major plant hormones. Acknowledgements Thanks to Jyan-Chyun Jang and Ken Feldmann for images of sterol and brassinosteroid-deficient mutants.
References 1. Hartmann M: Plant sterols and the membrane environment. Trends Plant Sci 1998, 3:170-175. 2. Edwards P, Ericsson J: Sterols and isoprenoids: signaling molecules derived from the cholesterol biosynthetic pathway. Annu Rev Biochem 1999, 68:157-185. 3. Clouse S, Sasse J: Brassinosteroids: essential regulators of plant growth and development. Annu Rev Plant Physiol Plant Mol Biol 1998, 49:427-451. 4. Clouse S, Feldmann K: Molecular genetics of brassinosteroid action. In Brassinosteroids: Steroidal Plant Hormones. Edited by Sakurai A, Yokota T, Clouse S. Tokyo: Springer; 1999:163-190.
R604
Current Biology Vol 10 No 16
5. Gachotte D, Meens R, Benveniste P: An Arabidopsis mutant deficient in sterol biosynthesis: heterologous complementation by ERG3 encoding a ∆7-C-5-desaturase from yeast. Plant J 1995, 8:407-416. 6. Choe S, Noguchi T, Fujioka S, Takatsuto S, Tissier C, Gregory B, Ross A, Tanaka A, Yoshida S, Tax F, Feldmann K: The Arabidopsis dwf7/ste1 mutant is defective in the ∆7 sterol C-5 desaturation step leading to brassinosteroid biosynthesis. Plant Cell 1999, 11:207-221. 7. Jang J-C, Fujioka S, Tasaka M, Seto H, Takatsuto S, Ishii A, Aida M, Yoshida S, Sheen J: A critical role of sterols in embryonic patterning and meristem programming revealed by the fackel mutant of Arabidopsis thaliana. Genes Dev 2000, 14:1485-1497. 8. Schrick K, Mayer U, Horrichs A, Kuhnt C, Bellini C, Dangl J, Schmidt J, Jurgens G: FACKEL is a sterol C-14 reductase required for organized cell division and expansion in Arabidopsis embryogenesis. Genes Dev 2000, 14:1471-1484. 9. Diener A, Li H, Zhou W-X, Whoriskey W, Nes W, Fink G: STEROL METHYLTRANSFERASE 1 controls the level of cholesterol in plants. Plant Cell 2000, 12:853-870. 10. Mayer U, Torres-Ruiz R, Berleth T, Misera S, Jurgens G: Mutations affecting the body organization in the Arabidopsis embryo. Nature 1991, 353:402-407.
R601
Plant development: A role for sterols in embryogenesis Steven D. Clouse
The Arabidopsis mutants fackel and sterol methyltransferase 1 have defects associated with body organization of the seedling. Molecular analysis of these mutants has revealed that plant sterols may be key signaling molecules influencing position-dependent cell fate during embryonic development. Address: Department of Horticultural Science, North Carolina State University, Raleigh, North Carolina 27695-7609, USA. Current Biology 2000, 10:R601–R604 0960-9822/00/$ – see front matter © 2000 Elsevier Science Ltd. All rights reserved.
Sterols are isoprenoid-derived compounds that play essential roles in the development of all eukaryotic organisms. Bulk sterols, such as cholesterol in animals, ergosterol in yeast and sitosterol and campesterol in plants, are integral membrane components which serve to regulate the fluidity and permeability of membranes and directly affect the activity of membrane associated proteins, including enzymes and signal transduction components [1]. These same sterols also serve as biosynthetic precursors of steroid hormones, including mammalian androgens, estrogens and glucocorticoids; insect ecdysteroids; fungal antheridiol and oogoniol; and plant brassinosteroids. Moreover, recent evidence from animal studies suggests that, in addition to the well-known mechanism of steroid hormone action, sterols can themselves serve as ligands for nuclear receptors and interact with other transcription complexes to directly modulate signal transduction pathways [2]. Given the multiple and critical roles that sterols play, it is not surprising that mutations in genes encoding sterol biosynthetic enzymes can have a dramatic affect on eukaryotic development. Four plant mutants with lesions in the sterol biosynthetic pathway have now been identified, in addition to five mutants known to have defects in the specific pathway leading to brassinosteroids. Comparison of the phenotypes of these mutants and their responses to brassinosteroid application is revealing an intriguing story about the roles that sterols and their hormone derivatives play in controlling both embryonic and post-embryonic plant development. The critical importance of brassinosteroids in plant growth and development became apparent in recent years as a result of combined molecular genetic and biochemical analyses [3]. Brassinolide, the most active brassinosteroid, is derived from campesterol via a series of sidechain hydroxylations combined with ring reductions, oxidations and epimerizations. Mutants affected in several steps of
this pathway have been identified, including constitutive photomorphogenesis and dwarfism (cpd ), dwarf4 (dwf4) and de-etiolated2 (det2). These mutants show a characteristic phenotype in the light, including dwarf stature, dark green and rounded leaves, prolonged life-span, reduced fertility and altered vascular development. In the dark, they exhibit features of light-grown plants, including shortened hypocotyl and open cotyledons [4]. All of these phenotypic alterations can be rescued by exogenous application of brassinolide. Mutants with defects in the sterol biosynthetic pathway preceding campesterol have also been identified. A screen of ethyl-methanesulfonate-mutagenized Arabidopsis seedlings by gas chromatography uncovered a mutant, ste1 [5], that accumulated ∆7 sterols with a decrease in the corresponding ∆5 sterols. Transgenic plants expressing the yeast ERG3 gene, which encodes a ∆7-C-5-desaturase, regained the normal sterol profile. The ste1 mutant first identified apparently carried a weak or leaky allele, as it showed no visible phenotype. A null allele of ste1, dwarf7 (dwf7) was discovered in a screen for dwarfs in a population of T-DNA-mutagenized Arabidopsis plants. This mutant had many of the phenotypic features of brassinosteroiddeficient mutants (although not as severe), which could be rescued to wild-type by brassinosteroid treatment [6]. Feeding experiments with labeled intermediates showed that the dwf7 mutant accumulated episterol, while 5-dehydroepisterol was not detected. This, coupled with significant sequence similarity of the DWF7 gene product to yeast C-5 desaturases, showed that the dwf7/ste1 lesions occur in the gene encoding ∆7-C-5desaturase. Similar types of analysis showed that the allelic mutants dwarf1/dimunito/cabbage1 (dwf1/dim/cbb1) are defective in the conversion of 24-methylenecholesterol to campesterol (reviewed in [4]). These mutants share many of the phenotypic characteristics of dwf7, including intermediate dwarfism and rescue to wild-type by brassinosteroid treatment. Three recent papers [7–9] have identified mutants with blocks very early in the sterol biosynthetic pathway that have some of the characteristics of brassinosteroiddeficient mutants as adult plants, but show unique defects during embryogenesis not previously seen in brassinosteroid mutants or sterol biosynthetic mutants affected later in the pathway. Moreover, these mutants are not rescued by brassinosteroid treatment. The fackel mutant of Arabidopsis was initially identified in a systematic screen for mutations affecting body organization in
R602
Current Biology Vol 10 No 16
Arabidopsis seedlings [10]. The extra-long-lifespan mutant was uncovered in a genetic screen for constitutive cytokinin response mutants, and subsequent analysis revealed that extra-long-lifespan is an allele of fackel [7]. Molecular characterization of the fackel mutants by two independent groups has provided strong evidence that the FACKEL gene encodes a sterol C-14 reductase required for the conversion of 4α-methyl-5α-ergosta8,14,24(28)-trien-3β-ol to 4α-methylfecosterol [7,8]. The FACKEL protein shows significant sequence similarity to animal and fungal C-14 sterol reductases, and FACKEL cDNA was found to rescue the defective sterol C-14 reductase in the yeast mutant erg24. Furthermore, the levels of brassinosteroids, campesterol and sitosterol were found to be severely reduced in the mutant, whereas the sterol C-14 reductase substrate had accumulated to ten times its wild-type level. Interestingly, the fackel mutant accumulates three unusual 8,14-diene sterols, as also observed in plant cell suspension cultures treated with 15-azasterol, an inhibitor of sterol C-14 reductase. The sterol methyltransferase 1 (smt1) mutant of Arabidopsis shares many of the phenotypic properties of fackel and has been shown to have a defect in a step very early in the sterol biosynthetic pathway [9]. The SMT1 gene encodes an enzyme capable of C-24 alkylation of the sterol side chain in the presence of S-adenosylmethionine, and recombinant SMT1 protein was found to catalyse the conversion of cycloartenol to 24-methylene cycloartenol. Cholesterol accumulates in the smt1 mutant at the expense of sitosterol, although other sterol levels are relatively normal. During development of the Arabidopsis embryo, cell fate is determined in a position-dependent manner, generating an apical–basal pattern along the main body axis and a series of concentric rings in a radial pattern around the main axis. Several distinct stages of embryogenesis can be distinguished, including globular, heart and torpedo stages. Embryogenesis was found to be severely disrupted in fackel mutants, starting with a lack of asymmetrical cell division in the globular-stage embryo. While wild-type embryos progress to the heart stage, fackel embryos remain globular and disorganized. Multiple shoot apical meristems are initiated in the fackel mutant, and developing seedlings often have more than the normal two cotyledons. The cotyledons appear to be directly attached to the root, with little development of the hypocotyl (Figure 1); root development itself is also altered. In situ hybridization showed that the FACKEL gene is prominently expressed in wild-type plants during embryo development [8]. The smt1 mutant [9] shows similar defects in embryogenesis to the fackel mutant, and the wild-type gene shows similar expression levels. As mentioned above, adult fackel plants exhibit many of the
features of brassinosteroid-deficient mutants — and are themselves brassinosteroid-deficient — but they cannot be rescued by brassinosteroid treatment, even though they retain some sensitivity to brassinosteroids [7]. Why do plants compromised early in the sterol biosynthetic pathway show severe defects in embryogenesis, while those affected later in the pathway, such as dwf7/ste1 and dwf1/dim1, do not? The simple reduction in bulk sterols, such as sitosterol and campesterol, cannot be the only answer, as dwf7 and dwf1 also have reduced sterol levels but do not show the same defects. Furthermore, fackel is not rescued by treatment with high levels of these sterols and smt1 has relatively normal levels of campesterol [9]. One possibility is that the unusual sterols that accumulate in the mutants become incorporated into membranes, altering their properties. Basic cell division is not affected in the fackel mutant, however, as mutant callus cells proliferate and cell-expansion defects in the embryo are not observed until the globular stage, by when about 60 cells have undergone division [8]. This argues against the notion that a general membrane defect disturbs cell division and expansion in these mutants. An intriguing possibility is that a sterol molecule itself serves as a signal that controls pattern formation within the embryo. This sterol could be one of the intermediates in the pathway between the product of the C-14 reductase and the substrate of the ∆7-C-5-desaturase, or these sterols might serve as precursors for as-yet unidentified sterols or nonbrassinosteroid hormones. The unusual sterols accumulated in the mutants could also act as signals, although the fact the fackel and smt1 have similar embryonic phenotypes, but accumulate different sterols, argues against this. A role for non-steroid hormone sterols in signaling has precedence in the animal kingdom. Hedgehog proteins are a family of signaling molecules crucial in early development of invertebrates and vertebrates. Both Drosophila Hedgehog and mouse Sonic hedgehog have been shown to undergo a covalent modification with cholesterol that is essential for proper spatial patterning during embryogenesis. Other examples include the activation of meiosis in mammalian cells by the cholesterol precursors 4,4-dimethyl-5α-cholesta-8,14,24trien-3β-ol and 4,4-dimethyl-5α-cholesta-8,14,24-dien-3βol, and the activation of nuclear receptors by oxysterols such as 25-, 26- and 27-hydroxycholesterol [2]. Brassinosteroids have become well-established signaling molecules required for normal post-embryonic plant development. The molecular analyses of fackel and smt1 mutants have raised the exciting possibility that other compounds of the sterol biosynthetic pathway may play a hormonal-like role in controlling embryogenesis and position-dependent cell fates. The ready availability of
Dispatch
R603
Figure 1 Biosynthetic pathways of sterols and brassinosteroids required for normal plant development. Cycloartenol, a polycyclic sterol intermediate unique to plants, is alkylated at C-24 by sterol methyltransferase 1, and converted to the trien form in a series of steps. The trien is reduced by the FACKEL gene product, a C-14 sterol reductase, to yield 4α-methylfecosterol, which then proceeds via a split pathway to the bulk membrane sterols sitosterol and campesterol in several steps, including a desaturation and C-24 reduction. Campesterol also serves as the progenitor of brassinosteroids, which are required for normal post-embryonic development. Defects in embryogenesis observed in the fackel mutant suggest that a non-brassinosteroid sterol intermediate might serve as a signal for proper pattern formation in the developing embryo. (a) Morphological differences between wild-type (left) and fackel (right) embryos at the heart stage. (b) An adult fackel mutant shows some of the characteristics of brassinosteroid-deficient mutants. (c) The fackel mutant often has multiple cotyledons and no apparent hypocotyl. (d) Several unique dien sterols accumulate in the fackel mutant (with the same ring structure as the C-14 reductase substrate).
Mevalonic acid
(d)
(a)
(b)
HO
5α-Cholesta8,14-dien-3β-ol (24R)-5α-Ergosta8,14,-dien-3β-ol
(c)
(24R)-5α-Stigmasta8,14-dien-3β-ol
Cycloartenol
fackel
C-14 sterol reductase
HO
HO
4α-Methyl-5α-ergosta-8,14,24(28)-trien-3β-ol
4α-Methylfecosterol
Citrostadienol
24-Methylenelophenol
Avenasterol
Episterol
dwf7/ste1 (∆7 Sterol C-5-desaturase)
5-Dehydroavenasterol
5-Dehydroepisterol
Isofucosterol
24-Methylenecholesterol dwf1/dim (C-24 reductase)
HO
HO
HO
Sitosterol
Stigmasterol
det2
Campesterol dwf4 cpd
Membrane sterols Brassinosteroids
Wild type
Current Biology
genetic and biochemical tools make it likely that progress in uncovering these factors will be much more rapid than the seventeen-year span that elapsed between discovery of the structure of brassinolide and the acceptance of brassinosteroids as major plant hormones. Acknowledgements Thanks to Jyan-Chyun Jang and Ken Feldmann for images of sterol and brassinosteroid-deficient mutants.
References 1. Hartmann M: Plant sterols and the membrane environment. Trends Plant Sci 1998, 3:170-175. 2. Edwards P, Ericsson J: Sterols and isoprenoids: signaling molecules derived from the cholesterol biosynthetic pathway. Annu Rev Biochem 1999, 68:157-185. 3. Clouse S, Sasse J: Brassinosteroids: essential regulators of plant growth and development. Annu Rev Plant Physiol Plant Mol Biol 1998, 49:427-451. 4. Clouse S, Feldmann K: Molecular genetics of brassinosteroid action. In Brassinosteroids: Steroidal Plant Hormones. Edited by Sakurai A, Yokota T, Clouse S. Tokyo: Springer; 1999:163-190.
R604
Current Biology Vol 10 No 16
5. Gachotte D, Meens R, Benveniste P: An Arabidopsis mutant deficient in sterol biosynthesis: heterologous complementation by ERG3 encoding a ∆7-C-5-desaturase from yeast. Plant J 1995, 8:407-416. 6. Choe S, Noguchi T, Fujioka S, Takatsuto S, Tissier C, Gregory B, Ross A, Tanaka A, Yoshida S, Tax F, Feldmann K: The Arabidopsis dwf7/ste1 mutant is defective in the ∆7 sterol C-5 desaturation step leading to brassinosteroid biosynthesis. Plant Cell 1999, 11:207-221. 7. Jang J-C, Fujioka S, Tasaka M, Seto H, Takatsuto S, Ishii A, Aida M, Yoshida S, Sheen J: A critical role of sterols in embryonic patterning and meristem programming revealed by the fackel mutant of Arabidopsis thaliana. Genes Dev 2000, 14:1485-1497. 8. Schrick K, Mayer U, Horrichs A, Kuhnt C, Bellini C, Dangl J, Schmidt J, Jurgens G: FACKEL is a sterol C-14 reductase required for organized cell division and expansion in Arabidopsis embryogenesis. Genes Dev 2000, 14:1471-1484. 9. Diener A, Li H, Zhou W-X, Whoriskey W, Nes W, Fink G: STEROL METHYLTRANSFERASE 1 controls the level of cholesterol in plants. Plant Cell 2000, 12:853-870. 10. Mayer U, Torres-Ruiz R, Berleth T, Misera S, Jurgens G: Mutations affecting the body organization in the Arabidopsis embryo. Nature 1991, 353:402-407.