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Spermidine, but not spermine, is essential for pigment pattern formation in zebrafish.

Frohnhöfer HG, Geiger-Rudolph S, Pattky M, Meixner M, Huhn C, Maischein HM, Geisler R, Gehring I, Maderspacher F, Nüsslein-Volhard C, Irion U - Biol Open (2016)

Bottom Line: Here we identify idefix, a mutation in the zebrafish gene encoding the enzyme spermidine synthase, leading to a severe reduction in spermidine levels as shown by capillary electrophoresis-mass spectrometry.This allows us to uncouple them from events occurring later during colour patterning.Thus, zebrafish provide a vertebrate model to study the in vivo effects of polyamines.

View Article: PubMed Central - PubMed

Affiliation: Max-Planck-Institut für Entwicklungsbiologie, Abteilung 3, Spemannstrasse 35, Tübingen 72076, Germany.

No MeSH data available.


Related in: MedlinePlus

Development of the exocrine pancreas is defective in ide mutants. Expression of trypsin in 72 hpf embryos visualized by in situ hybridization. (A) heterozygous (ide+/−) and (B) homozygous (ide−/− zyg. only, maternal contribution present) mutants derived from heterozygous parents show no defects (n=40). Whereas (C) homozygous mutants derived from an incross of homozygous fish, i.e. zygotic mutants with no maternal contribution (ide−/− mat. & zyg.), show a severe reduction in the expression domain, indicating defects in the development of the exocrine pancreas (n=24). Scale bar: 0.1 mm.
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BIO018721F6: Development of the exocrine pancreas is defective in ide mutants. Expression of trypsin in 72 hpf embryos visualized by in situ hybridization. (A) heterozygous (ide+/−) and (B) homozygous (ide−/− zyg. only, maternal contribution present) mutants derived from heterozygous parents show no defects (n=40). Whereas (C) homozygous mutants derived from an incross of homozygous fish, i.e. zygotic mutants with no maternal contribution (ide−/− mat. & zyg.), show a severe reduction in the expression domain, indicating defects in the development of the exocrine pancreas (n=24). Scale bar: 0.1 mm.

Mentions: Recently a critical role for polyamine biosynthesis, especially spermidine, in the growth and differentiation of the pancreas in zebrafish was reported (Mastracci et al., 2015). To investigate the effects of the ide mutation on the development of the exocrine pancreas we used in situ hybridization and assessed the expression of the trypsin gene (try), which is specifically expressed in differentiated exocrine cells of the pancreas. We found that homozygous ide embryos derived from homozygous parents (maternal-zygotic mutants) showed a very strong reduction in the trypsin-expressing region, indicating a severe reduction in the size of the exocrine pancreas (Fig. 6). In contrast, zygotic mutant embryos derived from crosses of heterozygous females with homozygous males, showed no difference in try expression compared to their heterozygous siblings. This demonstrates that the eggs are maternally provided with spermidine synthase mRNA or the enzyme itself, and that the enzymatic function is critical for embryonic development.Fig. 6.


Spermidine, but not spermine, is essential for pigment pattern formation in zebrafish.

Frohnhöfer HG, Geiger-Rudolph S, Pattky M, Meixner M, Huhn C, Maischein HM, Geisler R, Gehring I, Maderspacher F, Nüsslein-Volhard C, Irion U - Biol Open (2016)

Development of the exocrine pancreas is defective in ide mutants. Expression of trypsin in 72 hpf embryos visualized by in situ hybridization. (A) heterozygous (ide+/−) and (B) homozygous (ide−/− zyg. only, maternal contribution present) mutants derived from heterozygous parents show no defects (n=40). Whereas (C) homozygous mutants derived from an incross of homozygous fish, i.e. zygotic mutants with no maternal contribution (ide−/− mat. & zyg.), show a severe reduction in the expression domain, indicating defects in the development of the exocrine pancreas (n=24). Scale bar: 0.1 mm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4920196&req=5

BIO018721F6: Development of the exocrine pancreas is defective in ide mutants. Expression of trypsin in 72 hpf embryos visualized by in situ hybridization. (A) heterozygous (ide+/−) and (B) homozygous (ide−/− zyg. only, maternal contribution present) mutants derived from heterozygous parents show no defects (n=40). Whereas (C) homozygous mutants derived from an incross of homozygous fish, i.e. zygotic mutants with no maternal contribution (ide−/− mat. & zyg.), show a severe reduction in the expression domain, indicating defects in the development of the exocrine pancreas (n=24). Scale bar: 0.1 mm.
Mentions: Recently a critical role for polyamine biosynthesis, especially spermidine, in the growth and differentiation of the pancreas in zebrafish was reported (Mastracci et al., 2015). To investigate the effects of the ide mutation on the development of the exocrine pancreas we used in situ hybridization and assessed the expression of the trypsin gene (try), which is specifically expressed in differentiated exocrine cells of the pancreas. We found that homozygous ide embryos derived from homozygous parents (maternal-zygotic mutants) showed a very strong reduction in the trypsin-expressing region, indicating a severe reduction in the size of the exocrine pancreas (Fig. 6). In contrast, zygotic mutant embryos derived from crosses of heterozygous females with homozygous males, showed no difference in try expression compared to their heterozygous siblings. This demonstrates that the eggs are maternally provided with spermidine synthase mRNA or the enzyme itself, and that the enzymatic function is critical for embryonic development.Fig. 6.

Bottom Line: Here we identify idefix, a mutation in the zebrafish gene encoding the enzyme spermidine synthase, leading to a severe reduction in spermidine levels as shown by capillary electrophoresis-mass spectrometry.This allows us to uncouple them from events occurring later during colour patterning.Thus, zebrafish provide a vertebrate model to study the in vivo effects of polyamines.

View Article: PubMed Central - PubMed

Affiliation: Max-Planck-Institut für Entwicklungsbiologie, Abteilung 3, Spemannstrasse 35, Tübingen 72076, Germany.

No MeSH data available.


Related in: MedlinePlus