Disease relevance of Sycp3

• In addition, embryo death in SCP3-deficient females increases with advancing maternal age [1].

High impact information on Sycp3

• Offspring derived from murine Sycp3(-)(/)(-) females die in utero as a result of aneuploidy [2].
• We show that DNA double-stranded breaks are inefficiently repaired in Sycp3(-)(/)(-) oocytes, thereby generating a temporal spectrum of recombination errors [2].
• The synaptonemal complex protein 3 (SYCP3) transiently supports the structural organization of the meiotic chromosome axis [2].
• We propose that SCP3 fibers constitute the core of the lateral elements of the synaptonemal complex and function as a molecular framework to which other proteins attach, regulating DNA binding to the chromatid axis, sister chromatid cohesion, synapsis, and recombination [3].
• Here, we show that the postmigratory germ cell-specific genes Mvh, Dazl and Scp3 are demethylated in germ cells, but not in somatic cells [4].

Biological context of Sycp3

• Here, we show at the EM level that in Sycp3(-/-) spermatocyte chromosomes lack the AE and the conical end thickening, but still they attach their telomeres to the inner NM with an electron-dense plate that contains T(2)AG(3) repeats [5].
• Bouquet stage spermatocytes were approximately threefold enriched, and the number of telomere but not centromere signals was reduced to the haploid in advanced Sycp3(-/-) spermatocytes, which indicates a special mode of homolog pairing at the mammalian telomere [5].
• Sycp3-null female mice produce aneuploid oocytes, which after fusion with normal haploid sperm, result in offspring with systemic whole chromosome, aneuploid embryo cells [6].
• Using the Sycp3-null female as a model, we observe an increase in the number of embryonic cells at E7.0 that exhibit abnormal chromosomal bridges at the anaphas estage of mitosis [6].
• In order to gain insights into the behavior of germ cells around this period and into likely mechanisms controlling entry into meiosis, we have studied by wholemount in situ hybridization the expression pattern of two germ cell-specific markers, Oct4 and Sycp3, during mouse fetal gonad development [7].

Anatomical context of Sycp3

• We have analysed the spatial distribution of cohesin-complex proteins associated with meiotic chromosomes in germ cells derived from Sycp3-deficient female and male mice [8].
• Staining of cell squashes from day 19 testes with anti-gamma-H2AX and anti-SCP3 antibodies showed that germ cells from DazlKO males were unable to progress beyond the leptotene stage of meiotic prophase I [9].

Other interactions of Sycp3

• We have analysed the behaviour of SCP3 and the cohesin subunit Rad21 in mouse spermatocytes by means of a squashing technique [10].
• We find that whereas SYCP3 is expressed in germ cell-like cells, other meiotic proteins, such as SYCP1, SYCP2, STAG3 (stromal antigen 3), REC8 (meiotic protein similar to the rad21 cohesins), and SMC1 (structural maintenance of chromosomes-1)-beta, are not expressed [11].
• SCP3 is a meiosis-specific structural protein appearing at axial elements and lateral elements of the synaptonemal complex [10].
• We observed a dynamic wave of expression of both genes in developing ovaries, with Oct4 expression being extinguished in a rostro-caudal wave and Sycp3 being upregulated in a corresponding wave, during the period 13.5-15.5 dpc [7].
• The Rad51 foci in mouse spermatocytes appear after the emergence of, and attached to, short chromosomal core segments that we visualize with Cor1-specific antibody [12].

Analytical, diagnostic and therapeutic context of Sycp3

• Fluorescence in situ hybridization with mouse chromosome 8- and 12-specific subsatellite probes uncovered reduced levels of regional homolog pairing, whereas painting of chromosomes 13 revealed partial or complete juxtapositioning of homologs; however, condensation of Sycp3(-/-) bivalents was defective [5].
• Immunofluorescence detected telomere proteins, SCP2, and the meiosis-specific cohesin STAG3 at the Sycp3(-/-) telomere [5].

References