In addition, we provided evidence that the expression pattern of miR-29a in DG area is similar to that of NeuN (mature neuronal marker), which suggested that miR-29a is increased during neuron maturation.
In contrast, in F. angustifolia, 85.17 % of sites were C3-C4 marker, which suggested that F. angustifolia belong to the C3-C4 species (Table 2).
Surprisingly, besides finding Olig2+ nuclei co-expressing NG2 and PDGFRα, many other Olig2+ nuclei did not express either cell surface marker, which suggests that Olig2+ cells might have differentiated to the oligodendroglial lineage and silenced the expression of NG2 and/or PDGFRα.
This is fewer than in past estimates based on demographic reconstructions and simpler genetic analyses, for example those based on blood group markers, which suggested the founding group had about 100-1000 breedindividualsuals.
Considering the intestinal-type pulmonary histology and multiple colonic polyps, we evaluated on the tissue of the proband the MSI markers, which suggested the absence of microsatellite instability (MSS phenotype).
ANO1 was expressed in small sensory neurons and was highly colocalized with nociceptor markers, which suggests that it may be involved in nociception.
RFLP markers generated multiple loci more often than microsatellite markers, which suggests that microsatellite markers are more suitable than RFLP markers as consensus markers.
The histone marker profiles showed two different peaks of combined nine histone markers, which suggests these two opposite genes had differently regulatory regions.
Finally, investigators found that epidemic V. cholerae isolates all shared the same molecular markers, which suggests that a point introduction had occurred.
A more careful analysis revealed that these regions had markers with very low levels of linkage disequilibrium with neighboring markers, which suggests potential mapping or assembly issues in the reference genome.
These results indicate that markers explained an important part of polygenic additive variance, however, about half of the genetic variance was not explained by the markers, which suggests the need for developing higher density SNP panels for genotyping.
