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However, we also found a distinct subpopulation of embryos whose lethality at early post-implantation stages could be explained only by a previously unknown defect in gametogenesis originating from Tek-driven Ate1 deletion in premeiotic germs cells.
The dose of morpholino for each gene was initially titrated to reduce lethality at early stages of development (not shown).
Hmga1 might compensate the Hmga2-KO, thereby avoiding lethality at early embryonic stages, as is the case after Gata6-KO [ 31, 32], or soon after birth due to defects in the lung, as is the case after lung epithelium-specific ablation of Gata6[ 11].
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We observed that early TIAR overexpression led to low transgene transmission associated with embryonic lethality starting at early post-implantation stages.
Complete loss of the HSD10 protein in mouse embryos causes lethality at very early stages of embryogenesis (day 5 p.f).
In C. elegans vinculin deficiency leads to the loss of muscular activity and lethality at an early larval stage (Barstead and Waterston, 1989).
In mice, deletion of PTEN results in lethality at the early stages of gastrulation before somitogenesis [15], but the detailed effects on differentiation and migration of cells have not been identified.
In the mouse, targeted disruption of the S1P-encoding gene Mbtps1 prevented normal epiblast formation and subsequent implantation of the embryo (Mitchell et al. 2001), resulting in lethality at an early developmental stage (Yang et al. 2001).
Polδ absence caused lethality at an earlier embryonic stage than these aforementioned DNA polymerases.
In the mouse, double mutants for Pitx1 and Pitx2 lead to early lethality (at pre- or peri-implantation stages) of the embryo (Marcil et al., 2003).
ADAM10-deficient mice have been generated [ 11], but their early lethality at day E9.5 prevents a reliable analysis of ADAM10's α-secretase function in vivo, especially in neuronal cells.
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