14 research outputs found
Analyse moleculaire d'un retrotransposon dont l'expression est modulee par une hormone steroiede
SIGLECNRS T Bordereau / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc
Asymmetric flies: The control of developmental noise in Drosophila
International audienceWhat are the sources of phenotypic variation and which factors shape this variation are fundamental questions of developmental and evolutionary biology. Despite this simple formulation and intense research, controversy remains. Three points are particularly discussed: (1) whether adaptive developmental mechanisms buffering variation exist at all; (2) if yes, do they involve specific genes and processes, i.e., different from those involved in the development of the traits that are buffered?; and (3) whether different mechanisms specifically buffer the various sources of variation, i.e., genetic, environmental and stochastic, or whether a generalist process buffers them all at once. We advocate that experimental work integrating different levels of analysis will improve our understanding of the origin of phenotypic variation and thus help answering these contentious questions. In this paper, we first survey the current views on these issues, highlighting potential sources of controversy. We then focus on the stochastic part of phenotypic variation, as measured by fluctuating asymmetry, and on current knowledge about the genetic basis of developmental stability. We report our recent discovery that an individual gene, Cyclin G, plays a central roleadaptive or notin developmental stability in Drosophila.(1) We discuss the implications of this discovery on the regulation of organ size and shape, and finally point out open questions
Data from: Phenotypic plasticity through transcriptional regulation of the evolutionary hotspot gene tan in Drosophila melanogaster
Phenotypic plasticity is the ability of a given genotype to produce different phenotypes in response to distinct environmental conditions. Phenotypic plasticity can be adaptive. Furthermore, it is thought to facilitate evolution. Although phenotypic plasticity is a widespread phenomenon, its molecular mechanisms are only beginning to be unravelled. Environmental conditions can affect gene expression through modification of chromatin structure, mainly via histone modifications, nucleosome remodelling or DNA methylation, suggesting that phenotypic plasticity might partly be due to chromatin plasticity. As a model of phenotypic plasticity, we study abdominal pigmentation of Drosophila melanogaster females, which is temperature sensitive. Abdominal pigmentation is indeed darker in females grown at 18°C than at 29°C. This phenomenon is thought to be adaptive as the dark pigmentation produced at lower temperature increases body temperature. We show here that temperature modulates the expression of tan (t), a pigmentation gene involved in melanin production. t is expressed 7 times more at 18°C than at 29°C in female abdominal epidermis. Genetic experiments show that modulation of t expression by temperature is essential for female abdominal pigmentation plasticity. Temperature modulates the activity of an enhancer of t without modifying compaction of its chromatin or level of the active histone mark H3K27ac. By contrast, the active mark H3K4me3 on the t promoter is strongly modulated by temperature. The H3K4 methyl-transferase involved in this process is likely Trithorax, as we show that it regulates t expression and the H3K4me3 level on the t promoter and also participates in female pigmentation and its plasticity. Interestingly, t was previously shown to be involved in inter-individual variation of female abdominal pigmentation in Drosophila melanogaster, and in abdominal pigmentation divergence between Drosophila species. Sensitivity of t expression to environmental conditions might therefore give more substrate for selection, explaining why this gene has frequently been involved in evolution of pigmentation
raw data Fig8 and S6Fig
tan relative expression in control females and trx RNAi females, ChIP for H3K4me3 in control females and trx RNAi females, abdominal pigmentation quantification in control females (w1118) and females mutant for trx
raw data Fig2
Expression of pigmentation genes in abdominal epidermis of female pharates and adults grown at 18°C and 29°
raw data S5Fig
IP H3/input, IP H3K27ac/Input and IP H3K4me3/IP H3 in abdominal epidermis of females grown at 18°C and 29°
raw data S4Fig
Relative expression of vg and CG12119 in abdominal epidermis of w1118 females grown at 18°C and 29°
raw data Fig4 and S2Fig
Quantification of abdominal pigmentation of tan mutant and control females grown at 18°C, 25°C and 29°C
raw data S6Fig
Relative expression of pigmentation genes in control females (RNAi GFP) and RNAi trx female
raw data S3Fig
GFP quantification in abdominal segments of ebony-nEGFP females grown at 18°C and 29°