Petal pigmentation patterning is widespread in flowering plants. The genetics of these pattern elements has been of great interest for understanding the evolution of phenotypic diversification. Here, we investigate the genetic changes responsible for the evolution of an unpigmented petal element on a colored background. We used transcriptome analysis, gene expression assays, cosegregation in F2plants and functional tests to identify the gene(s) involved in petal coloration in We identified an R2R3‐MYB transcription factor (CgsMYB12) responsible for anthocyanin pigmentation of the basal region (‘cup’) in the petal of Distinct spatial patterns of
- NSF-PAR ID:
- 10223427
- Editor(s):
- Bomblies, K
- Date Published:
- Journal Name:
- Genetics
- Volume:
- 217
- Issue:
- 2
- ISSN:
- 1943-2631
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Summary Clarkia gracilis ssp.sonomensis .C .gracilis ssp.sonomensis . A functional mutation inCgsMYB12 creates a white cup on a pink petal background. Additionally, we found that twoR2R3‐MYB genes (CgsMYB6 andCgsMYB11 ) are also involved in petal background pigmentation. Each of these threeR2R3‐MYB genes exhibits a different spatiotemporal expression pattern. The functionality of theseR2R3‐MYB genes was confirmed through stable transformation ofArabidopsis .R2R3‐MYB expression have created the possibility that pigmentation in different sections of the petal can evolve independently. This finding suggests that recent gene duplication has been central to the evolution of petal pigmentation patterning inC. gracilis ssp.sonomensis . -
The origin of phenotypic novelty is a perennial question of genetics and evolution. To date, few studies of biological pattern formation specifically address multi-generational aspects of inheritance and phenotypic novelty. For quantitative traits influenced by many segregating alleles, offspring phenotypes are often intermediate to parental values. In other cases, offspring phenotypes can be transgressive to parental values. For example, in the model organism Mimulus (monkeyflower), the offspring of parents with solid-colored petals exhibit novel spotted petal phenotypes. These patterns are controlled by an activator-inhibitor gene regulatory network with a small number of loci. Here we develop and analyze a model of hybridization and pattern formation that accounts for the inheritance of a diploid gene regulatory network composed of either homozygous or heterozygous alleles. We find that the resulting model of multi-generational Turing-type pattern formation can reproduce transgressive petal phenotypes similar to those observed in Mimulus. The model gives insight into how non-patterned parent phenotypes can yield phenotypically transgressive, patterned offspring, aiding in the development of empirically testable hypotheses.more » « less
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The origin of phenotypic novelty is a perennial question of genetics and evolution. To date, few studies of biological pattern formation specifically address multi-generational aspects of inheritance and phenotypic novelty. For quantitative traits influenced by many segregating alleles, offspring phenotypes are often intermediate to parental values. In other cases, offspring phenotypes can be transgressive to parental values. For example, in the model organism Mimulus (monkeyflower), the offspring of parents with solid-colored petals exhibit novel spotted petal phenotypes. These patterns are controlled by an activator-inhibitor gene regulatory network with a small number of loci. Here we develop and analyze a model of hybridization and pattern formation that accounts for the inheritance of a diploid gene regulatory network composed of either homozygous or heterozygous alleles. We find that the resulting model of multi-generational Turing-type pattern formation can reproduce transgressive petal phenotypes similar to those observed in Mimulus. The model gives insight into how non-patterned parent phenotypes can yield phenotypically transgressive, patterned offspring, aiding in the development of empirically testable hypotheses.more » « less
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Abstract The origin of phenotypic novelty is a perennial question of genetics and evolution. To date, few studies of biological pattern formation specifically address multi-generational aspects of inheritance and phenotypic novelty. For quantitative traits influenced by many segregating alleles, offspring phenotypes are often intermediate to parental values. In other cases, offspring phenotypes can be transgressive to parental values. For example, in the model organism
Mimulus (monkeyflower), the offspring of parents with solid-colored petals exhibit novel spotted petal phenotypes. These patterns are controlled by an activator-inhibitor gene regulatory network with a small number of loci. Here we develop and analyze a model of hybridization and pattern formation that accounts for the inheritance of a diploid gene regulatory network composed of either homozygous or heterozygous alleles. We find that the resulting model of multi-generational Turing-type pattern formation can reproduce transgressive petal phenotypes similar to those observed inMimulus . The model gives insight into how non-patterned parent phenotypes can yield phenotypically transgressive, patterned offspring, aiding in the development of empirically testable hypotheses. -
Summary Patterned leaf coloration in plants generates remarkable diversity in nature, but the underlying mechanisms remain largely unclear.
Here, using
Medicago truncatula leaf marking as a model, we show that the classicM. truncatula leaf anthocyanin spot trait depends on two R2R3 MYB paralogous regulators, RED HEART1 (RH1) and RH2.RH1 mainly functions as an anthocyanin biosynthesis activator that specifically determines leaf marking formation depending on its C‐terminal activation motif. RH1 physically interacts with the
M. truncatula bHLH protein MtTT8 and the WDR family member MtWD40‐1, and this interaction facilitates RH1 function in leaf anthocyanin marking formation. RH2 has lost transcriptional activation activity, due to a divergent C‐terminal domain, but retains the ability to interact with the same partners, MtTT8 and MtWD40‐1, as RH1, thereby acting as a competitor in the regulatory complex and exerting opposite effects. Moreover, our results demonstrate that RH1 can activate its own expression and that RH2‐mediated competition can repressRH1 expression.Our findings reveal the molecular mechanism of the antagonistic gene paralogs RH1 and RH2 in determining anthocyanin leaf markings in
M. truncatula , providing a multidimensional paralogous–antagonistic regulatory paradigm for fine‐tuning patterned pigmentation.