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This tail defect was tMO1-dose dependent (Fig. 4D).
While the embryos show a minor posterior tail defect, the body trunk and gross head/brain structure are relatively normal.
Of these, two exhibited craniorachischisis (example shown in Fig. 3A), whereas the third had hindbrain exencephaly and a tail defect (Fig. 3B; supplementary material Table S3).
Other double mutants exhibited exencephaly (n=1/32; 3%; Fig. 2F) or had only a tail defect (Fig. 2G; n=2/32) or no overt defect (n=2/32).
The tail defect in zebrafish pax9 morphants could be rescued only by zebrafish pax9 mRNA, while the aberrant phenotype could not be rescued by mRNA of members of the same subfamily, pax1a and pax1b.
Other defects seen in Scrib Crc /+; Celsr1 Crsh /+ fetuses included lumbosacral open spina bifida (2%, n=1/41; Fig. 2K) or isolated exencephaly (7%, n=3/41; Fig. 2L), although many appeared phenotypically normal (46%, n=19/41; Fig. 2M) or had only a tail defect (2%, n=1/41).
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To define by transmission electron microscopy (TEM) analysis, the prevalence of sperm tail defects of genetic origin among men suffering for a reduced or absent sperm motility.
The same trend followed all other defects: tail defects, sperm head defects and other defects.
Sperm defects that can be seen include tail defects, loose heads and distal droplets [ 40].
Tail defects and loss of movement/escape responses were scored from Stage 30 and gut coiling defects from Stage 40.
The lowest percentage of spermatozoa with tail defects was detected at the beginning of the experiment (19.44 ± 22.96 %, Figure 2).
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