Figure 8: Centrosome aberrations are detected in seminoma tissue with abnormally low LGALS3BP levels.

(a) RT–PCR quantification of different human tumour tissues was used to identify tissues with deregulated LGALS3BP levels when compared with relevant control tissue. The strongest deregulation is present in testis, where the expression of LGALS3BP is eight-fold downregulated in the seminoma (boxed). Immunoblotting, haematoxylin staining analysis and immunofluorescence microscopy for corresponding tissue samples are shown in b–d. (b) Immunoblotting of the control testis tissue shows normal LGALS3BP protein levels, which are abnormally reduced in seminoma cancer tissue. α-tubulin and β-actin were used as loading controls. (c) Haematoxylin-stained cryosection of testis (i) and seminoma (ii) tissue. Seminoma with sheet-like arrangement of cells with clear cytoplasm, well-defined cell membranes, and nuclei with prominent, central nucleoli. Tumour nodules are subdivided by branching, fibrous septa containing few lymphocytes. Normal testis with clusters of Leydig cells. Seminiferous tubules are lined by Sertoli cells. Occasional representation of spermatogenesis. Scale bars, 200 μm. (d) Cryosections of human testis control tissue (first row) and human seminoma tissue (second row). The control tissue shows both normal-sized centrioles and PCM, whereas in the seminoma aberrant, centriolar structures are detected with and without associated PCM. In the composite images, anti-centrin labelling is shown in green, γ-tubulin in red and DAPI-stained DNA in blue. Scale bars, 5 μm. In the third row, confocal microscopy image projections of double-labelled mitotic cells in seminoma tissue with phosphorylated Histone H3 (red) and γ-tubulin (green) are shown. Inserts on the bottom of each image show an enlarged view of the centrosome. Abnormally distributed chromosomes are frequently detected in cells correlating with aberrant shaped centrosomes. (e) Model describing the interrelation between deregulation of LGALS3BP and PLK4-dependent centriolar structure accumulation and PCM hypertrophy, respectively.