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Gene Review:

him-8 - Protein HIM-8

Caenorhabditis elegans

Phillips, C.M. et al., Nelms, B.L. et al., Broverman, S.A. et al., Goldstein, P., Goldstein, P. et al., et al.

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Disease relevance of him-8

Their occurrence in pachytene nuclei is independent of the mechanism responsible for nondisjunction, i.e. point mutations as in him-8 versus chromosomal aberrations as in mnT6 [1].

High impact information on him-8

The him-8 gene is essential for proper meiotic segregation of the X chromosomes in C. elegans [2].
Surprisingly, a point mutation in him-8 that retains both chromosome binding and NE localization fails to stabilize pairing or promote synapsis [2].
Here we show that loss of him-8 function causes profound X chromosome-specific defects in homolog pairing and synapsis. him-8 encodes a C2H2 zinc-finger protein that is expressed during meiosis and concentrates at a site on the X chromosome known as the meiotic pairing center (PC) [2].
Moreover, we conclude that suppression of egl-13 is due to a meiosis-independent function of him-8 because suppression is observed in mutants that have severely reduced meiotic germ cell populations and suppression does not depend on the function of him-8 in the maternal germ line [3].
Interactions between these genes can give insight into function of Sox family members, which are important in many aspects of metazoan development, and into functions of him-8 outside of meiosis [3].

Associations of him-8 with chemical compounds

In the present study, high incidence of male (him) mutants, him-5 and him-8, were treated with dimethyl sulfone (DMSO2), the primary metabolite of dimethyl sulfoxide (DMSO) [4].

Other interactions of him-8

Recessive mutations in three autosomal genes, him-1, him-5 and him-8, cause high levels of X chromosome nondisjunction in hermaphrodites of Caenorhabditis elegans, with no comparable effect on autosomal disjunction [5].
This is also true in him-4 and him-8 in which case there are 3 and zero SC knobs in the hermaphrodites, respectively, and one SC knob each in the male pachytene nuclei [6].
(v) Three meiotic mutants, him-3, him-6, and him-8, had no effect on somatic loss of the duplications but did reduce the frequency of breakage events [7].

References

The synaptonemal complexes of Caenorhabditis elegans: the dominant him mutant mnT6 and pachytene karyotype analysis of the X-autosome translocation. Goldstein, P. Chromosoma (1986) [Pubmed]
HIM-8 binds to the X chromosome pairing center and mediates chromosome-specific meiotic synapsis. Phillips, C.M., Wong, C., Bhalla, N., Carlton, P.M., Weiser, P., Meneely, P.M., Dernburg, A.F. Cell (2005) [Pubmed]
C. elegans HIM-8 functions outside of meiosis to antagonize EGL-13 Sox protein function. Nelms, B.L., Hanna-Rose, W. Dev. Biol. (2006) [Pubmed]
Effects of dimethyl sulfone (DMSO2) on early gametogenesis in Caenorhabditis elegans: ultrastructural aberrations and loss of synaptonemal complexes from pachytene nuclei. Goldstein, P., Magnano, L., Rojo, J. Reprod. Toxicol. (1992) [Pubmed]
Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans. Broverman, S.A., Meneely, P.M. Genetics (1994) [Pubmed]
The synaptonemal complexes of Caenorhabditis elegans: pachytene karyotype analysis of male and hermaphrodite wild-type and him mutants. Goldstein, P. Chromosoma (1982) [Pubmed]
Spontaneous duplication loss and breakage in Caenorhabditis elegans. McKim, K.S., Rose, A.M. Genome (1994) [Pubmed]

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