Project description:The individualization of serially repeated homologs is one route through which novel traits are thought to evolve. Under this model, a repeated character—like a limb, digit, or sensory bristle—is individualized from its homologs by changes in the regulatory apparatus (‘character identity network’, ChIN) that specifies its development. Individualization then enables downstream gene networks that build the repeated character to diverge from one another in different parts of the body, ultimately allowing new phenotypic endpoints to be reached. Despite this model’s intuitive appeal, the genetic mechanisms through which new ChINs rewire trait-building gene networks remain largely uncharacterized. A promising system in which to study this process is the Drosophila sex comb. Found in a sublineage of Drosophila species, the sex comb is a recently evolved, male-specific innovation that evolved from a more evolutionarily ancient precursor—the mechanosensory (MS) bristle—following the gain of a novel ChIN centered on the sex determination gene dsx and HOX gene Scr. Here, we use time-series single-cell RNA-seq to show that rather than co-opting new genes, this new ChIN orchestrates quantitative and heterochronic changes in the ancestral MS bristle transcriptome. These changes affect gene modules that control energy metabolism, endoreplication, and actin dynamics. The net effect of these changes is an organ-specific shift in developmental rate, leading to accelerated growth in sex comb teeth. Collectively, our work suggests that morphological innovation can proceed without the co-option of new genes into downstream trait-building networks and instead through metabolically driven differences in developmental rate between serial homologs.
2026-02-12 | GSE293356 | GEO
Project description:Transcriptome sequencing of Mythimna separata ovipositor bristle zone
Project description:A total of 18 libraries from Setaria viridis were constructed using the Illumina TruSeq sample preparation method. We used two biological replicate libraries from the leaf, whole panicles (inside leaf sheath), whole panicles (coming out of leaf sheath), whole panicles (completely out of leaf sheath), whole panicles (completely out of leaf sheath, after pollination), spikelet (inside leaf sheath), spikelet (coming out of leaf sheath), and spikelet (completely out of leaf sheath).
Project description:Diversity in cytoskeleton organization and function may be achieved through alternative tubulin isotypes and by a variety of post-translational modifications. The Drosophila genome contains five different β-tubulin paralogs, which may play an isotype tissue-specific function in vivo. One of these genes, the beta-tubulin60D gene, which is expressed in a tissue-specific manner, was found to be essential for fly viability and fertility. To further understand the role of the beta-tubulin60D gene, we generated new beta-tubulin60D null alleles (beta-tubulin60DM) using the CRISPR/Cas9 system and found that the homozygous flies were viable and fertile. Moreover, using a combination of genetic complementation tests, rescue experiments, and cell biology analyses, we identified Pin1, an unknown dominant mutant with bristle developmental defects, as a dominant-negative allele of beta-tubulin60D. We also found a missense mutation in the Pin1 mutant that results in an amino acid replacement from the highly conserved glutamate at position 75 to lysine (E75K). Analyzing the β-tubulin structure suggests that this E75K alteration destabilizes the alpha-helix structure and may also alter the GTP-Mg2+ complex binding capabilities. Our results revisited the credence that beta-tubulin60D is required for fly viability and revealed for the first time in Drosophila, a novel dominant-negative function of missense beta-tubulin60D mutation in bristle morphogenesis