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lhp1 mutants are early flowering and have curled leaf morphology [26] thus sharing some phenotypic traits with curly leaf (clf) mutants affected in a PRC2 core component.
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The mutants were early flowering with short flowering period.
The D30A and D30N mutant proteins were early successes in this study.
The de-repression of FLC and MAFs in clf, emf2 and FIE-suppressed plants was expected to lead to late flowering because the elevated expression of these genes alone causes late flowering [3], [4], [13]; however, these mutant plants all are early-flowering [47], [52], [55].
The mutants are characterized by earlier expression of genes associated with cell wall biosynthesis and a decrease in photosynthetic genes in late stages.
Despite the differences in assays of apoptosis, the dynamics of the linker histone mutants are consistent with earlier studies and the modified recombinants were comparable to the parent proteins (in the presence or absence of Bak-Bcl-xL Bak-Bcl-xL Bak-Bcl-xLomatin compaction functionsuggestingHs were nothatanged.
Twinfilin localization at the tips of all stereocilia of whirler mutants was observed early as postnatal day 7 (supplemental data Fig. S2).
Of the 6 misclassified cancers that had sequencing verified mutations, 5 were missense mutants and half were early stage.
Besides the reddish brown pigmentation of the leaf midrib and stalk pith associated with lignified tissues, brown-midrib (bm) mutants of maize were early distinguished by their lower lignin content and modified lignin structure [ 5- 7].
lin-35; pha-1 double mutants are defective at an early step in pharyngeal morphogenesis leading to an abnormal pharyngeal architecture.
We thus find that morphological defects in ablated mutants are first seen at early somitic stages.
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