Sentence examples for mutant embryos have from inspiring English sources

Zebrafish swirl (bmp2) mutant embryos have abnormal dorso-ventral patterning and lack cardiac progenitors marked by Nkx2.5 expression [8].

Those melanophores that do develop in trpm7 single mutant embryos have punctate cell morphology upon differentiation, in contrast to the transiently stellate cell morphology of enz melanophores.

OFT alignment defects in Hes1 mutant embryos have been independently observed by another group who, in addition, noted aortic arch artery abnormalities associated with a defective smooth muscle contribution at E11.5 (P. Scambler, personal communication).

At E14.5, the expected Mendelian ratio (1/16) of double mutant was obtained (15/231), indicating the STAT5/Gab2 double mutant embryos have no overall survival disadvantage at this stage of development.

Whereas mutant mice for Hey2 (also known as CHF1, Herp1, Hrt2, Hesr2 or gridlock in zebrafish) show no obvious vascular abnormalities with multiple cardiac defects [4] [6], compound Hey1; Hey2 mutant embryos have impaired arterial-venous specification [7], [8], similar to those seen in mutant mice for Notch receptors and ligands, including Dll4 [9]–[11].

Zyap1 −/− mutant embryos have fewer cells compared to sibling controls.

In contrast, only 9 of 104 NMJ sections (9%) from Df 3R Exel6191 mutant embryos had synapses.

At later stages, no mutant embryos had LPM expression (n = 14).

In comparison, crn-6 tm890) crn-6 tm890yos had an average 10.2, 11.0 and 0.7 TUNEL-positive signals, whereas crn-7(ok866) mutant embryos had only 6.0, 6.9 and 0.4 TUNEL-positive nuclei, averagecomma, 10.2fold, and 4-fold embryonic stages, respectively.

Only 4/14 mutant embryos had expression in the left atrium of the heart, 2 of which had dextrally looped hearts.

We showed that as previously reported, h47 mutant embryos had no patterning defect, and yet, extra TCs were specified.