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. Author manuscript; available in PMC: 2016 Mar 3.
Published in final edited form as: Cell Rep. 2015 Feb 26;10(8):1252–1260. doi: 10.1016/j.celrep.2015.01.060

Figure 3. Mature somatic inclusions bear the hallmarks of human Lewy pathology.

Figure 3

Mature Syn-GFP inclusions are heavily phosphorylated at serine-129 (A1–4), in an amyloid dye binding configuration (A1–2) and ubiquitinated (A3). The green fluorescence from these inclusions is due to the presence of Syn-GFP and not an endogenous autofluorescent species, since they colabel with antibody to GFP (A4). Similar mature inclusions made only of untagged endogenous mouse alpha-synuclein (A5) are also present in nearby neurons that do not express Syn-GFP. These inclusions share a similar morphology and modification state to Syn-GFP-positive ones. Syn-GFP levels within mature inclusions (B, arrow) are greatly increased over levels of the protein in nearby neurons without inclusions (arrowhead). Colocalization of Syn-GFP with serine-129 phosphorylated alpha-synuclein (B) is also increased in inclusions versus cells without inclusions. N = cells/animals. Individual neurons from human frontal cortex in cases of Dementia with Lewy Bodies (C) are stained with hematoxylin to outline the nuclei in blue and for serine-129 phospho-synuclein aggregates in brown. Two examples demonstrate wrapping of aggregated alpha-synuclein around the nucleus (C1–2), similar to that seen in mature mouse inclusions. Two other examples show “legs” of the inclusion that wrap around the nucleus (C3–4, black arrowhead), also similar to mature mouse inclusions. Scale bar 5 µm. See also Fig. S1&2.