TY - JOUR
T1 - BEN domain protein Elba2 can functionally substitute for linker histone H1 in Drosophila in vivo
AU - Xu, Na
AU - Lu, Xingwu
AU - Kavi, Harsh
AU - Emelyanov, Alexander V.
AU - Bernardo, Travis J.
AU - Vershilova, Elena
AU - Skoultchi, Arthur I.
AU - Fyodorov, Dmitry V.
N1 - Funding Information:
We are grateful to E. Lai for fly stocks and V. Corces for antibodies. We thank S. Buhl and M. Scharff for raising mouse polyclonal antibodies. We also thank K. Beirit and A. Konev for helpful discussions and critical reading of the manuscript. This work was supported by grants from the National Institutes of Health to D.V.F. (GM074233) and A.I.S. (GM093190 and GM116143). N.X. was supported in part by the NIH IRACDA/K12 training grant (K12GM102779). T.J.B. was supported in part by a NIH F32 Fellowship (GM115210).
PY - 2016/9/30
Y1 - 2016/9/30
N2 - Metazoan linker histones are essential for development and play crucial roles in organization of chromatin, modification of epigenetic states and regulation of genetic activity. Vertebrates express multiple linker histone H1 isoforms, which may function redundantly. In contrast, H1 isoforms are not present in Dipterans, including D. melanogaster, except for an embryo-specific, distantly related dBigH1. Here we show that Drosophila BEN domain protein Elba2, which is expressed in early embryos and was hypothesized to have insulator-specific functions, can compensate for the loss of H1 in vivo. Although the Elba2 gene is not essential, its mutation causes a disruption of normal internucleosomal spacing of chromatin and reduced nuclear compaction in syncytial embryos. Elba2 protein is distributed ubiquitously in polytene chromosomes and strongly colocalizes with H1. In H1-depleted animals, ectopic expression of Elba2 rescues the increased lethality and ameliorates abnormalities of chromosome architecture and heterochromatin functions. We also demonstrate that ectopic expression of BigH1 similarly complements the deficiency of H1 protein. Thus, in organisms that do not express redundant H1 isoforms, the structural and biological functions performed by canonical linker histones in later development, may be shared in early embryos by weakly homologous proteins, such as BigH1, or even unrelated, non-homologous proteins, such as Elba2.
AB - Metazoan linker histones are essential for development and play crucial roles in organization of chromatin, modification of epigenetic states and regulation of genetic activity. Vertebrates express multiple linker histone H1 isoforms, which may function redundantly. In contrast, H1 isoforms are not present in Dipterans, including D. melanogaster, except for an embryo-specific, distantly related dBigH1. Here we show that Drosophila BEN domain protein Elba2, which is expressed in early embryos and was hypothesized to have insulator-specific functions, can compensate for the loss of H1 in vivo. Although the Elba2 gene is not essential, its mutation causes a disruption of normal internucleosomal spacing of chromatin and reduced nuclear compaction in syncytial embryos. Elba2 protein is distributed ubiquitously in polytene chromosomes and strongly colocalizes with H1. In H1-depleted animals, ectopic expression of Elba2 rescues the increased lethality and ameliorates abnormalities of chromosome architecture and heterochromatin functions. We also demonstrate that ectopic expression of BigH1 similarly complements the deficiency of H1 protein. Thus, in organisms that do not express redundant H1 isoforms, the structural and biological functions performed by canonical linker histones in later development, may be shared in early embryos by weakly homologous proteins, such as BigH1, or even unrelated, non-homologous proteins, such as Elba2.
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U2 - 10.1038/srep34354
DO - 10.1038/srep34354
M3 - Article
AN - SCOPUS:84989923410
VL - 6
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 34354
ER -