The NF-κB signaling pathway was suspected to be crucially involved in the development of naturally occurring Treg cells, because mice lacking molecules of proximal TCR signaling leading to NF-κB activation, such as PCKθ, Bcl10, or CARMA1, show marked defects in the thymic generation of Treg cells [48], [49], [50], [51].
However, the axonal arborizations of mutant PNs in the protocerebrum manifested marked defects.
Injection of 25 pg of full length Mef2ca 4–5–6 RNA had dramatic effects on embryonic development, inducing lethality in approximately 30% of the embryos and marked developmental defects in 49% of the surviving embryos, classified as 'severely defective' (Fig. S6A,B).
Moreover, we observed that prometaphase chromosomes isolated from two-cell stage embryos show in 20% of cells (7/36) a marked cohesion defect at the centromeres.
The synthetic lethal phenotypes found in double mutants of Dcas and Src or FAK56D were marked by defects in dorsal closure and in some cases by the appearance of anterior cuticle holes that suggested head involution defects.
However, at the stage of flowering, elp6 mop2 RP40p::PIN1 still exhibits marked morphological defects.
In a minority of patients on treatment there are marked functional defects, especially in killing activity.
Secondly, in the surviving otd null single cell clones of the ALl1 lineage, we did not see any marked targeting defects.
A previous report showed similar findings in a zebrafish model, wherein blockade of spg11 expression presented outgrowth defects together with a marked reduction of acetylated tubulin (17).
Also, loss of Fli1 in adult mice resulted in mild thrombocytopenia associated with a marked reduction of megakaryocytic progenitors and maturation defect of megakaryocytes present in bone marrow.
