Exact(2)
This loss of ovarian BicD resulted in a decrease in embryonic BicD (Fig. 1F); BicD in t = 1 embryos was approximately 1.6% that in wildtype embros (Fig. 1G).
Moreover, exploration of the role of I2 in Drosophila development evidenced that an I2 loss-of-function in mothers leads to a dramatic reduction in the viability of progeny as measured by a decrease in embryonic hatch rates and larval lethality.
Similar(58)
However, by E7.5, there was a 23%and32%2% decrease in embryonic height and width, respectively (p < 0.005; Figure 2B), suggesting a failure to increase the rate of proliferation in the epiblast that normally occurs at the onset of gastrulation (Mac Auley et al., 1993; Snow, 1977).
The increase in GFP+ embryos correlated with a 64% average decrease in embryonic viability, consistent with autosome missegregation (Hodgkin 2005).
While we do not know whether these cellular hallmarks are responsible for the observed increased lethality beyond the thermal limits, we note that a mere 10% decrease in embryonic viability is associated with readily observable cellular changes during the first cell cycle.
Although expressed in the mouse posterior fossa mesenchyme, loss of Foxc1 non-autonomously induces a rapid and devastating decrease in embryonic cerebellar ventricular zone radial glial proliferation and concurrent increase in cerebellar neuronal differentiation.
Local mIGF1 expression led also to an attenuation of the switch in myosin heavy chain (MHC) isoform expression associated with SRF loss, with a significant increase in the level of postnatal α-MHC mRNA and a trend towards a decrease in the amount of embryonic β-MHC mRNAs (Fig. 3A).
That is, compared with control counterparts, a decrease in the mRNA expression of embryonic and neonatal MHC was detected in phenotype stage Smn −/− ; SMN2 mice, while these transcripts were increased in Smn 2B/− samples at P21.
Specifically, a positive net effect could explain the increase in embryonic volume, observed at E13.5, yet, a negative – or inhibitory – net effect could, in turn, explain the decrease in embryonic volume, observed at E17.5.
We also note that there remains the possibility that some of the apparent decrease in embryonic droplets reflects increased basal droplet localization, to a central area of the embryo where droplet quantitation is difficult.
Germiller and Goldstein [20] observed a decrease in proliferation of chondrocytes in the avian embryonic growth plate as a result of immobilization, and proposed that skeletal muscle contractions play a role in the regulation of immature chondrocytes.
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