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R2R3 MYB proteins in Class II underwent duplication in the Arabidopsis lineage, though the duplicates have apparently retained roles in regulating SCW biosynthesis.
The chromosomal location of the duplication events showed that part of chromosomes 2 and 4 underwent duplication events that resulted in the duplication of REM IX genes, a class of B3 genes exclusive to Arabidopsis (Figure 5).
The phylogeny of the B3 proteins of all species included in this work indicated that the putative ancestor of the B3 domain is similar to B3 domain of green algae and underwent duplication and evolved to the ABI3 and HSI gene families in plants.
The phylogenetic tree of B3 proteins for each family shows that many genes of the ABI3, HSI, ARF, RAV and REM families have underwent duplication events after the split between bryophytes and angiosperms, monocots and eurosids, and eurosids I and eurosids II, showing that the expansion of the B3 superfamily occurred in several stages (Figure 9).
TR genes underwent duplication independently in the Protostomia and Deuterostomia.
The metazoan CSL genes (class M) obviously underwent duplication too.
Similar(14)
Ten supergroups were defined that separated prior to the bryophyte/tracheophyte split and subsequently underwent duplications, giving rise to at least 32 groups that separated prior to the monocot/eudicot split.
Additionally, our analysis uncovered B3 genes from other families that have underwent recent duplication in different chromosomes, as well as old duplication events (Table S6).
According to this hypothesis, boule underwent gene duplication during vertebrate evolution, generating the autosomal dazl, which underwent further duplications, producing additional copies that were translocated to the Y-chromosome in primates [1].
During the vertebrate evolution, boule underwent gene duplication, producing the autosomal dazl, which duplicated further, leading to additional copies that were translocated to the Y-chromosome in catarrhine primates and amplified to multiple daz genes [15].
With further investigation using these linked read data, the FGFR2 copy number alteration was determined to be a deletion-inversion motif that underwent tandem duplication, with unique breakpoints in each metastasis.
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