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WMISH at 16 ts revealed greatly reduced Sry signal in Gadd45γ−/− mutant gonads when compared to wild-type controls.
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Mutant gonads appeared normal and there were no discrepancies observed between phenotypic (gonadal) sex and genotypic (chromosomal) sex.
One abnormality that was observed in Map3k1ΔKD homozygous embryos was an increased length of mutant gonads at 13.5 dpc.
In this report we show a quantitative and significant decrease of germ cell numbers in vivo, independent of sex, by E14.5 in Dazl−/− mutant gonads relative to wildtype.
Prior work identified >100 genes upregulated in spr-5 mutant gonads (Nottke et al. 2011).
Quantitation indicated an approximate 3.5-fold reduction in Sry levels in mutant gonads at this stage.
Also, ife-3 mutant gonads are smaller and contain fewer germ cells than those of wild-type animals (Fig. 4A,B).
The ovarian somatic marker, FOXL2, was also strongly induced in supporting cells of the XY mutant gonads at 14.5 dpc.
Analysis of the syncytial organization of adult lin-41 null mutant gonads indicates that the cytoplasmic core of the gonad narrows and terminates near the loop region, coincident with the premature cellularization of developing oocytes.
Class I mutant gonads had very few germ cells; class II mutants produced excess amounts of mitotic germ cells; and germ cells in the class III mutant hermaphrodites failed to switch from spermatogenesis to oogenesis (Fig. 1).
Disruption to cell proliferation in supporting cell precursors might arguably cause a reduction in the number of SRY-positive cells observed in mutant gonads, causing reduced Sry expression.
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