The rare stone marker was lost.
Immunofluorescence revealed that while nearly all EYFP+ acinar cells expressed the acinar marker carboxypeptidase A1 (CPA1) in controls, this marker was lost from approximately 15% of EYFP+ cells in Ptf1a cKO tissues, indicating loss of the normal differentiation state.
This was possible as most WS types have slightly different colony morphologies, which allow us to determine if the GFP marker was lost and the emergence of smooth ancestral types is easily detected.
Upon HR, the second selection marker is lost, whereas after integration by non-homologous recombination, transformants carrying both selectable markers are obtained.
It is very likely that this marker is lost after the cells become resident in the testis [ 48, 49].
If the selection marker is lost, pyrF transformants are unable to metabolize 5-FOA, thereby preventing cell death, and uracil in the plates would facilitate cell growth.
After 8 days of differentiation, Polycomb complex binding and the H3K27me3 marker were lost; however, there was no change in the DNA methylation pattern of the promoter, as has been previously reported in the case of other muscle genes [ 29].
When a dominant-negative form of lhx1 is expressed in the anterior kidney field, expression of proximal tubule markers is lost [30].
Only CD44+ cells expressed the pluripotency genes POU5F1, NANOG and SOX2 [27], [28], [29], [29], while these markers were lost in CD44− cells, suggesting that EMT may be involved in maintaining stemness.
When grown at low (clonal) density and switched into conditions that support differentiation, the precursor markers were lost and the cells acquired morphologies and antigen expression patterns found in neurons, astrocytes, and oligodendrocytes (Figure 1G H; Table 1).
GS cannot currently account for this scenario; thus, informative markers are lost.
