Fig. 8: RAD51B-c.92delT leads to a reduced reprogramming efficiency of MEFs and humanized Rad51b^KI/KI mice show an increased incidence of hyperplasia of the pituitary gland.

A MEFs from the indicated genotypes were infected with the 3 reprogramming factors and the numbers of alkaline phosphatase positive colonies were counted showing a significantly reduction (up to ~2 fold) in Rad51b-c.92delT homozygous mutant MEFs in comparison with the wild-type control. n = 9. Welch´s t-test analysis: ***p < 0.001. B Macroscopic image of adenohypophysis from Rad51b^WT/WT and adenohypophysis rom Rad51b^KI/KI mice. Reticulin staining (C–H) and Prolactin IHQ (I, J) of pituitary adenohypophysis from Rad51b^WT/WT and Rad51b^KI/KI. C, D Normal adenohypophysis from Rad51b^WT/WT show a reticulin staining pattern that is partially lost in zones of hyperplasia where the cell size is increased (magnified in D, indicated by an arrow). E, F Microadenoma from a Rad51b^KI/KI showing a complete loss of reticulin staining pattern that is still persistent in the neighbor misplaced adenohypophysis (magnified in F). G, H Macroadenoma from a Rad51b^KI/KI showing total loss of reticulin staining pattern and complete absence of normal adenohypophysis tissue. The neoplasm shows different adenoid and pseudopapillary growing patterns (magnified in H). I, J IHQ of prolactin in normal pituitary glands from Rad51b^WT/WT showing labelled cells unevenly distributed whereas adenomas from Rad51b^KI/KI revealed a high density of prolactin expressing cells. Bar in panels, 250 μm (C, E, G) and 50 μm (D, F, H, I, J). Rad51b^{c.92delT/c.92delT} variant is referred as Rad51b^KI/KI for simplicity.