Browsing by Issue Date, starting with "2017-09"
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- Diverse Cis-Regulatory Mechanisms Contribute to Expression Evolution of Tandem Gene DuplicatesPublication . Baudouin-Gonzalez, Luís; Santos, Marília A.; Tempesta, Camille; Sucena, Élio; Roch, Fernando; Tanaka, KohtaroPairs of duplicated genes generally display a combination of conserved expression patterns inherited from their unduplicated ancestor and newly acquired domains. However, how the cis-regulatory architecture of duplicated loci evolves to produce these expression patterns is poorly understood. We have directly examined the gene-regulatory evolution of two tandem duplicates, the Drosophila Ly6 genes CG9336 and CG9338, which arose at the base of the drosophilids between 40 and 60 million years ago. Comparing the expression patterns of the two paralogs in four Drosophila species with that of the unduplicated ortholog in the tephritid Ceratitis capitata, we show that they diverged from each other as well as from the unduplicated ortholog. Moreover, the expression divergence appears to have occurred close to the duplication event and also more recently in a lineage-specific manner. The comparison of the tissue-specific cis-regulatory modules (CRMs) controlling the paralog expression in the four Drosophila species indicates that diverse cis-regulatory mechanisms, including the novel tissue-specific enhancers, differential inactivation, and enhancer sharing, contributed to the expression evolution. Our analysis also reveals a surprisingly variable cis-regulatory architecture, in which the CRMs driving conserved expression domains change in number, location, and specificity. Altogether, this study provides a detailed historical account that uncovers a highly dynamic picture of how the paralog expression patterns and their underlying cis-regulatory landscape evolve. We argue that our findings will encourage studying cis-regulatory evolution at the whole-locus level in order to understand how interactions between enhancers and other regulatory levels shape the evolution of gene expression.
- The sex-specific effects of diet quality versus quantity on morphology in Drosophila melanogasterPublication . Shingleton, Alexander W.; Masandika, Josephine R.; Thorsen, Lily S.; Zhu, Yuqing; Mirth, Christen K.Variation in the quality and quantity of nutrition is a major contributor to phenotypic variation in animal populations. Although we know much of how dietary restriction impacts phenotype, and of the molecular-genetic and physiological mechanisms that underlie this response, we know much less of the effects of dietary imbalance. Specifically, although dietary imbalance and restriction both reduce overall body size, it is unclear whether both have the same effect on the size of individual traits. Here, we use the fruit fly Drosophila melanogaster to explore the effect of dietary food versus protein-to-carbohydrate ratio on body proportion and trait size. Our results indicate that body proportion and trait size respond differently to changes in diet quantity (food concentration) versus diet quality (protein-to-carbohydrate ratio), and that these effects are sex specific. While these differences suggest that Drosophila use at least partially distinct developmental mechanisms to respond to diet quality versus quantity, further analysis indicates that the responses can be largely explained by the independent and contrasting effects of protein and carbohydrate concentration on trait size. Our data highlight the importance of considering macronutrient composition when elucidating the effect of nutrition on trait size, at the levels of both morphology and developmental physiology.
- Comment on Rohrscheib et al. 2016 "Intensity of mutualism breakdown is determined by temperature not amplification of Wolbachia genes"Publication . Chrostek, Ewa; Teixeira, LuisRohrscheib et al. (PLOS Pathogens, 2016) discuss the interaction between the pathogenicity of the wMel variant wMelPop, temperature and Octomom copy number. The effect of temperature on wMelPop pathogenicity was already reported in the original work on wMelPop. The absence of pathogenicity at low temperatures was also shown before. We have recently demonstrated, in Chrostek and Teixeira 2015, that Octomom copy number determines wMelPop pathogenicity.
- Effect of celastrol on bone structure and mechanics in arthritic ratsPublication . Cascão, Rita; Vidal, Bruno; Jalmari Finnilä, Mikko Arttu; Lopes, Inês Pascoal; Teixeira, Rui Lourenço; Saarakkala, Simo; Moita, Luis Ferreira; Fonseca, João EuricoRheumatoid arthritis (RA) is characterised by chronic inflammation leading to articular bone and cartilage damage. Despite recent progress in RA management, adverse effects, lack of efficacy and economic barriers to treatment access still limit therapeutic success. Therefore, safer and less expensive treatments that control inflammation and bone resorption are needed. We have previously shown that celastrol is a candidate for RA treatment. We have observed that it inhibits both interleukin (IL)-1β and tumor necrosis factor (TNF) in vitro, and that it has anti-inflammatory properties and ability to decrease synovial CD68+ macrophages in vivo. Herein our goal was to evaluate the effect of celastrol in local and systemic bone loss.
- A tissue-specific, Gata6-driven transcriptional program instructs remodeling of the mature arterial treePublication . Losa, Marta; Latorre, Victor; Andrabi, Munazah; Ladam, Franck; Sagerström, Charles; Novoa, Ana; Zarrineh, Peyman; Bridoux, Laure; Hanley, Neil A; Mallo, Moises; Bobola, NicolettaConnection of the heart to the systemic circulation is a critical developmental event that requires selective preservation of embryonic vessels (aortic arches). However, why some aortic arches regress while others are incorporated into the mature aortic tree remains unclear. By microdissection and deep sequencing in mouse, we find that neural crest (NC) only differentiates into vascular smooth muscle cells (SMCs) around those aortic arches destined for survival and reorganization, and identify the transcription factor Gata6 as a crucial regulator of this process. Gata6 is expressed in SMCs and its target genes activation control SMC differentiation. Furthermore, Gata6 is sufficient to promote SMCs differentiation in vivo, and drive preservation of aortic arches that ought to regress. These findings identify Gata6-directed differentiation of NC to SMCs as an essential mechanism that specifies the aortic tree, and provide a new framework for how mutations in GATA6 lead to congenital heart disorders in humans.