Evolution of Bmp16
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ABSTRACT:
PROVIDER: PRJEB24983 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Asymmetric paralog evolution between the “cryptic” gene Bmp16 and its well-studied sister genes Bmp2 and Bmp4
| PRJEB25510 | ENA
Project description:Studying the evolution of binding preferences for 30 paralog TF pairs in S.cerevisiae
2022-01-21 | GSE179430 | GEO
Project description:Cell lines geneticially engineered to undergo conditional asymmetric self-renewal were used to identify genes whose expression is asymmetric self-renewal associated (ASRA). Non-random sister chromatid segregation occurs concordantly with asymmetric self-renewal in these cell lines. Asymmetric self-renewal occurs when murine embryo fibroblasts that are otherwise p53-null are induced to express physiological levels of wildtype p53 protein (Asym). To distinguish p53-responsive genes that also require induction of asymmetric self renewal (i.e., ASRA genes) and/or non-random sister chromatid segregation for change, an additional control cell line, which continues to symmetrically self-renew (with random sister chromatid segregation) even when p53 is induced, was also compared (Symp53). This congenic cell line constitutively expresses the type II inosine monophosphate dehydrogenase (IMPDH II; the rate-limiting enzmye for guanine ribonucleotide biosynthesis) and, thereby, prevents p53-induced asymmetric self-renewal and non-random sister chromatid segregation. Three biological replicates of asymmetrically self-renewing cultures (Asym1-3) were compared with cultures that were symmetrically self-renewing - either because they did not express p53 (3 biological replicates, Sym1-3) or they expressed constitutive IMPDH II (i.e., not regulated by p53) as well as p53 (2 biological replicates, Symp53_1 and 2.)
2010-12-22 | E-GEOD-25334 | biostudies-arrayexpress
Project description:Cryptic genetic variants exert minimal or no phenotypic effects alone but have long been hypothesized to form a vast, hidden reservoir of genetic diversity that drives trait evolvability through epistatic interactions. This classical theory has been reinvigorated by pan-genome sequencing, which is continually exposing cis-regulatory variation, along with widespread gene duplications and paralog diversification as an underappreciated source of cryptic variation within gene families and the regulatory networks in which they function. However, empirical testing of this hypothesis has been hindered by intractable genetics, limited allelic diversity, and inadequate phenotypic resolution. Here, guided by natural and engineered cis-cryptic variants in a recently evolved paralogous pair, we identified an additional pair of redundant trans regulators, establishing a regulatory network that controls tomato inflorescence architecture. Exploiting an allelic spectrum of network components allowed a high-resolution dissection of a genotype-to-phenotype map, revealing how cryptic variants potentiate trait diversification. We combined coding mutations with a cis-regulatory allelic series in populations segregating for all four genes, systematically constructing gene dosage combinations across 216 genotypes and quantifying their effects on branching in 27,000 inflorescences. Our analysis revealed dose-dependent interactions within paralog pairs enhance branching, culminating in strong, synergistic, effects. However, modeling uncovered an unexpected layer of antagonism between paralog pairs, where accumulating mutations in one pair progressively diminished the effects of mutations in the other. Our results demonstrate how gene regulatory network architecture and complex dosage effects from paralog diversification converge to shape phenotypic space. Given the prevalence of paralog evolution in genomes, we propose that paralogous cryptic variation within regulatory networks elicits hierarchies of epistatic interactions, catalyzing bursts of phenotypic change.
2025-05-29 | GSE289537 | GEO
Project description:Well studied strain
| PRJNA29851 | ENA
Project description:Well studied isolate
| PRJNA29891 | ENA