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A genome-wide survey of sexually dimorphic expression of Drosophila miRNAs identifies the steroid hormone-induced miRNA let-7 as a regulator of sexual identity.

Fagegaltier D, König A, Gordon A, Lai EC, Gingeras TR, Hannon GJ, Shcherbata HR - Genetics (2014)

Bottom Line: Second, in the soma, X-linked miRNAs do not systematically rely on dosage compensation.Together, our findings place ecdysone and let-7 as modulators of a somatic systemic signal that helps establish and sustain sexual identity in males and females and differentiation in gonads.This work establishes the foundation for a role of miRNAs in sexual dimorphism and demonstrates that similar to vertebrate hormonal control of cellular sexual identity exists in Drosophila.

View Article: PubMed Central - PubMed

Affiliation: Howard Hughes Medical Institute, Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 fagegalt@cshl.edu halyna.shcherbata@mpibpc.mpg.de.

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Effects of dosage compensation on X-linked miRNAs expression. (A) Compensasome association at the 27 X-linked miRNA loci vary, with 15 miRNAs located in regions highly populated by compensasomes (high), three miRNAs with low MSL coverage and seven miRNAs residing in regions deprived of compensasomes. Two miRNAs loci in regions not covered by the arrays (undet.) could not be assessed. We observe no difference in MSL occupancy for miRNAs residing in intronic or intergenic regions. The level of expression of miRNAs in the absence of a functional dosage-compensation complex was examined in male salivary glands (green charts) and whole larvae (blue charts) mutant for msl3 (B) or mle (C). Of the six X-linked miRNAs expressed in these tissues, mir-304, mir-12, and mir-13b show the expected twofold decrease in all mutant samples compared to controls. MiRNA levels remain unchanged, however, for X-linked mir-979, mir-210, or mir-283. Autosomal mir-981, mir-100, or mir-1013 levels did not change. Mir-314 levels increase in msl3 mutant salivary glands and decrease in whole larvae. All miRNAs were tested in triplicates on two independent biological replicates. Values were normalized to the autosomal gene standard, Dspt4, whose levels remain unchanged between males, females, or compensasome mutants (Chiang and Kurnit 2003). We observe similar trends between male and female salivary glands miRNAs in wild-type Oregon-R and msl3 heterozygous mutant controls for all 10 miRNAs tested (mir-100, mir-979, mir-12, mir-314, mir-981, mir-210, mir-1013, mir-283, mir-13b, mir-304). Error bars represent standard deviations. P-values: (*) P < 0.05; (**) P < 0.005; (***) P < 0.0005. Calculations are provided in Table S11, Table S12, Table S13, Table S14, Table S15, and Table S16.
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fig2: Effects of dosage compensation on X-linked miRNAs expression. (A) Compensasome association at the 27 X-linked miRNA loci vary, with 15 miRNAs located in regions highly populated by compensasomes (high), three miRNAs with low MSL coverage and seven miRNAs residing in regions deprived of compensasomes. Two miRNAs loci in regions not covered by the arrays (undet.) could not be assessed. We observe no difference in MSL occupancy for miRNAs residing in intronic or intergenic regions. The level of expression of miRNAs in the absence of a functional dosage-compensation complex was examined in male salivary glands (green charts) and whole larvae (blue charts) mutant for msl3 (B) or mle (C). Of the six X-linked miRNAs expressed in these tissues, mir-304, mir-12, and mir-13b show the expected twofold decrease in all mutant samples compared to controls. MiRNA levels remain unchanged, however, for X-linked mir-979, mir-210, or mir-283. Autosomal mir-981, mir-100, or mir-1013 levels did not change. Mir-314 levels increase in msl3 mutant salivary glands and decrease in whole larvae. All miRNAs were tested in triplicates on two independent biological replicates. Values were normalized to the autosomal gene standard, Dspt4, whose levels remain unchanged between males, females, or compensasome mutants (Chiang and Kurnit 2003). We observe similar trends between male and female salivary glands miRNAs in wild-type Oregon-R and msl3 heterozygous mutant controls for all 10 miRNAs tested (mir-100, mir-979, mir-12, mir-314, mir-981, mir-210, mir-1013, mir-283, mir-13b, mir-304). Error bars represent standard deviations. P-values: (*) P < 0.05; (**) P < 0.005; (***) P < 0.0005. Calculations are provided in Table S11, Table S12, Table S13, Table S14, Table S15, and Table S16.

Mentions: To address whether dosage compensation controls miRNA expression directly on the X chromosome, we first examined whether X-linked miRNAs reside in regions bound by MSL-1 in ChIP–Chip experiments reported by Straub et al. (2008) in S2 cells and embryos. We note that X-linked miRNAs reside outside the primary “high affinity sites” defined in these studies and are therefore not primary strong binding sites for compensasomes. MSL-1 levels were further divided into high, medium, low, or MSL-1 absent subtypes (Figure 2A). With the exception of two miRNA loci residing in regions not addressed in this study, 67% of X-linked miRNA loci reside in regions bound by compensasomes, indicating that some miRNAs could be dosage compensated.


A genome-wide survey of sexually dimorphic expression of Drosophila miRNAs identifies the steroid hormone-induced miRNA let-7 as a regulator of sexual identity.

Fagegaltier D, König A, Gordon A, Lai EC, Gingeras TR, Hannon GJ, Shcherbata HR - Genetics (2014)

Effects of dosage compensation on X-linked miRNAs expression. (A) Compensasome association at the 27 X-linked miRNA loci vary, with 15 miRNAs located in regions highly populated by compensasomes (high), three miRNAs with low MSL coverage and seven miRNAs residing in regions deprived of compensasomes. Two miRNAs loci in regions not covered by the arrays (undet.) could not be assessed. We observe no difference in MSL occupancy for miRNAs residing in intronic or intergenic regions. The level of expression of miRNAs in the absence of a functional dosage-compensation complex was examined in male salivary glands (green charts) and whole larvae (blue charts) mutant for msl3 (B) or mle (C). Of the six X-linked miRNAs expressed in these tissues, mir-304, mir-12, and mir-13b show the expected twofold decrease in all mutant samples compared to controls. MiRNA levels remain unchanged, however, for X-linked mir-979, mir-210, or mir-283. Autosomal mir-981, mir-100, or mir-1013 levels did not change. Mir-314 levels increase in msl3 mutant salivary glands and decrease in whole larvae. All miRNAs were tested in triplicates on two independent biological replicates. Values were normalized to the autosomal gene standard, Dspt4, whose levels remain unchanged between males, females, or compensasome mutants (Chiang and Kurnit 2003). We observe similar trends between male and female salivary glands miRNAs in wild-type Oregon-R and msl3 heterozygous mutant controls for all 10 miRNAs tested (mir-100, mir-979, mir-12, mir-314, mir-981, mir-210, mir-1013, mir-283, mir-13b, mir-304). Error bars represent standard deviations. P-values: (*) P < 0.05; (**) P < 0.005; (***) P < 0.0005. Calculations are provided in Table S11, Table S12, Table S13, Table S14, Table S15, and Table S16.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig2: Effects of dosage compensation on X-linked miRNAs expression. (A) Compensasome association at the 27 X-linked miRNA loci vary, with 15 miRNAs located in regions highly populated by compensasomes (high), three miRNAs with low MSL coverage and seven miRNAs residing in regions deprived of compensasomes. Two miRNAs loci in regions not covered by the arrays (undet.) could not be assessed. We observe no difference in MSL occupancy for miRNAs residing in intronic or intergenic regions. The level of expression of miRNAs in the absence of a functional dosage-compensation complex was examined in male salivary glands (green charts) and whole larvae (blue charts) mutant for msl3 (B) or mle (C). Of the six X-linked miRNAs expressed in these tissues, mir-304, mir-12, and mir-13b show the expected twofold decrease in all mutant samples compared to controls. MiRNA levels remain unchanged, however, for X-linked mir-979, mir-210, or mir-283. Autosomal mir-981, mir-100, or mir-1013 levels did not change. Mir-314 levels increase in msl3 mutant salivary glands and decrease in whole larvae. All miRNAs were tested in triplicates on two independent biological replicates. Values were normalized to the autosomal gene standard, Dspt4, whose levels remain unchanged between males, females, or compensasome mutants (Chiang and Kurnit 2003). We observe similar trends between male and female salivary glands miRNAs in wild-type Oregon-R and msl3 heterozygous mutant controls for all 10 miRNAs tested (mir-100, mir-979, mir-12, mir-314, mir-981, mir-210, mir-1013, mir-283, mir-13b, mir-304). Error bars represent standard deviations. P-values: (*) P < 0.05; (**) P < 0.005; (***) P < 0.0005. Calculations are provided in Table S11, Table S12, Table S13, Table S14, Table S15, and Table S16.
Mentions: To address whether dosage compensation controls miRNA expression directly on the X chromosome, we first examined whether X-linked miRNAs reside in regions bound by MSL-1 in ChIP–Chip experiments reported by Straub et al. (2008) in S2 cells and embryos. We note that X-linked miRNAs reside outside the primary “high affinity sites” defined in these studies and are therefore not primary strong binding sites for compensasomes. MSL-1 levels were further divided into high, medium, low, or MSL-1 absent subtypes (Figure 2A). With the exception of two miRNA loci residing in regions not addressed in this study, 67% of X-linked miRNA loci reside in regions bound by compensasomes, indicating that some miRNAs could be dosage compensated.

Bottom Line: Second, in the soma, X-linked miRNAs do not systematically rely on dosage compensation.Together, our findings place ecdysone and let-7 as modulators of a somatic systemic signal that helps establish and sustain sexual identity in males and females and differentiation in gonads.This work establishes the foundation for a role of miRNAs in sexual dimorphism and demonstrates that similar to vertebrate hormonal control of cellular sexual identity exists in Drosophila.

View Article: PubMed Central - PubMed

Affiliation: Howard Hughes Medical Institute, Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 fagegalt@cshl.edu halyna.shcherbata@mpibpc.mpg.de.

Show MeSH
Related in: MedlinePlus