The duration of treatment varies (mainly the first trimester), doses and type of drugs are different, and most abnormalities are not typical they are most frequently developmental defects of the nervous, bone and skeletal systems, and ventricular and atrial septal defects.
Congenital heart defects (CHD) are the most common developmental defects in humans [ 1], affecting 6 8 out of 1,000 newborns [ 2– 5].
While the prf1-4 prf2-1 mutant showed the most compounded developmental defects, we saw a combination of single mutant phenotypes in the prf1-4 prf3-2 and the prf2-1 prf3-2 double mutants.
The most striking developmental defect is reduction in the size of the brain and eyes when observed at 1 dpf.
Most interestingly, the compound RXR and RAR knockout mice recapitulate most of the developmental defects observed in the RAR double mutants [ 24, 28], and RXRα-RAR is the major functional unit to mediate RA signaling during embryonic development [ 29].
Sirt1 deficient mice also display a number of developmental defects, most noticeably, irregular shaped eyes, evident in embryos as early as d16.5 [19] with adult mice often failing to open one or both eyelids [18], [19] and defective cardiac septation [19].
By E14.5, embryos displayed grave developmental defects, most likely due to insufficient oxygenation.
Unlike obvious birth defects, most developmental effects cannot be seen at birth or even later in life.
Knockdown of most RP genes causes developmental defects in the brain of zebrafish, indicating that the vast majority of RP functions are associated with nervous system development [ 29].
Hypothyroidism in newborns (congenital hypothyroidism) in iodine-sufficient regions is most commonly caused by developmental defects of the thyroid (thyroid dysgenesis) (Foley 2000).
