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We have previously found that the aggregation defect of JH.D cells may be explained by the lack of mRNA expression of adenylyl cyclase ACA, such that the mutant cells fail to set up the cAMP signaling system [9].
Indeed, in mosaic third larval instar wing discs containing large coldf02290 Minute+ clones, we observed that the cold mutant cells fail to accumulate the FasIII marker in their most apical part, unlike the surrounding wild type cells (Fig. 7A,A').
SRF/Mal signaling is essential for border cell migration, as mal mutant cells fail to migrate.
It has been shown that DNA-PKcs mutant cells fail to arrest replication following stress [ 66].
In contrast, we find that His C mutant cells fail to accumulate string transcripts when arrested in G2.
Some PKC1 mutant cells fail to enter stationary phase when stressed, continuing to grow and replicate their DNA in spite of severely limited resources.
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Under stress, however, the mtm1 mutant cells failed to elevate PtdIns5P underscoring the role of AtMTM1 in producing PtdIns5P.
Repetitive analyses revealed that ctf7 elg1 double mutant cells failed to synchronize in G1 with the same efficiency as either ctf7 or elg1 single mutant strains.
During earlier stages of tracheal migration, h22 mutant cells failed to migrate out and instead formed large clusters of internalized cells (Figure 2E and H).
However, intact chromosomes from all swi3 mutant cells failed to migrate into the gel at 1.5 h and 3 h during recovery, indicating that Swi3 is required for the recovery of DNA replication after fork breakage.
These mutant cells failed to progress beyond the G1 phase of the cell cycle after extended time periods (96 hours exposure to DOX) even though most single unbudded cells (70%) were viable when these cells were arrayed onto YPD medium without DOX (data not shown).
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