ABSTRACT: Link between coloration, behavior and gene expression in the brain suggests divergent camouflage strategies in a coral reef fish species pair.
Project description:Aposematism and warning coloration are common defense strategies used by animals to deter predators. Pestilential gregarious locusts display a striking black-brown pattern, which is presumed to be a form of warning coloration compared to green solitary locusts. However, the specific mechanisms involved in regulating this distinctive pattern are not yet understood. Here, we found that different amounts of β-carotene and β-carotene-binding protein (βCBP) complexes confer the black tergum and brown sternum of locust. The expression level of βCBP is regulated by the bZIP transcription factor ATF2, which is activated by protein kinase C alpha (PKCα) in response to crowding. Specifically, ATF2 is phosphorylated at Ser327 and translocates to the nucleus, where it binds to specific sites on the βCBP promoter and stimulates overexpression. Differential phosphorylation of ATF2 resulted in the divergent black and brown body coloration of gregarious locusts. The overexpression of βCBP in the sternum is essential for the accumulation of red pigments, which creates the sharp contrast between the black tergum and the brown sternum. This spatial variation in ATF2 phosphorylation levels allows locusts to adapt to changing environmental conditions and better evade predation.
Project description:Animal pigment patterns play important roles in behavior and, in many species, red coloration serves as an honest signal of individual quality in mate choice. Among Danio fishes, some species develop erythrophores, pigment cells that contain red ketocarotenoids, whereas other species, like zebrafish (D. rerio) only have yellow xanthophores. Here, we use pearl danio (D. albolineatus) to assess the developmental origin of erythrophores and their mechanisms of differentiation. We show that erythrophores in the fin of D. albolineatus share a common progenitor with xanthophores and maintain plasticity in cell fate even after differentiation. We further identify the predominant ketocarotenoids that confer red coloration to erythrophores and use reverse genetics to pinpoint genes required for the differentiation and maintenance of these cells. Our analyses are a first step towards defining the mechanisms underlying the development of erythrophore-mediated red coloration in Danio and reveal striking parallels with the mechanism of red coloration in birds.
Project description:Aging is a multifactorial process that results in progressive loss of regenerative capacity and tissue function while simultaneously favoring the development of a large array of age-related diseases. Evidence suggests that the accumulation of senescent cells in tissue promotes both normal and pathological aging. Oxic stress is a key driver of cellular senescence. Because symbiotic long-lived reef corals experience daily hyperoxic and hypoxic transitions, we hypothesized that these long-lived animals have developed specific longevity strategies in response to light. We analyzed transcriptome variation in the reef coral Stylophora pistillata during the day–night cycle and revealed a signature of the FoxO longevity pathway. We confirmed this pathway by immunofluorescence using antibodies against coral FoxO to demonstrate its nuclear translocation. Among genes that were specifically up- or downregulated on exposure to light, human orthologs of two “light-up” genes (HEY1 and LONF3) exhibited anti-senescence properties in primary human fibroblasts. Therefore, these genes are interesting candidates for counteracting skin aging. We propose a large screen for other light-up genes and an investigation of the biological response of reef corals to light (e.g., metabolic switching) to elucidate these processes and identify effective interventions for promoting healthy aging in humans.
Project description:Plumage color plays a prominent role in reproductive isolation and thus understanding the genetic basis of pigmentation patterns can provide critical insight into speciation. Subspecies of the dark-eyed junco (Junco hyemalis) show marked differences in melanic plumage coloration known to have evolved rapidly since the Last Glacial Maximum just 18,000 years ago. To understand this rapid radiation we studied the pigment composition and the genetic basis of coloration in two divergent subspecies, the slate-colored and Oregon juncos. We used HPLC and light microscopy to investigate pigment deposition patterns in feathers from four body areas. RNA-seq data generated under common garden experimental conditions were then used to compare the relative roles of differential gene expression in growing feathers and sequence divergence in loci expressed during feather development. Junco feathers were found to differ in eumelanin and pheomelanin content and distribution, producing a range of black, gray and brown colors. Transcriptomic data revealed marked regulatory differences among subspecies and among body-parts within subspecies in known melanin-pathway genes (including PMEL, TYR, TYRP1, OCA2, MLANA), but also in several novel or poorly known loci (EDAR, VPS33B, HPS1). Within subspecies, lighter feathers expressed less melanin synthesis genes, more ASIP, and showed differential expression of Wnt signaling genes. Feathers from different body regions also showed differential expression of Hox genes. The two subspecies differed in expression of ASIP and three other genes (MFSD12, KCNJ13, HAND2) previously associated with color development. Sequence variation in the expressed genes was not related to color differences between junco subspecies. Our findings suggest that differential expression of a few genes can account for marked differences in plumage color and pattern, a mechanism that can account for the rapid diversification of juncos. Several novel candidate pigmentation genes found in juncos may contribute to the expression of melanic coloration in other vertebrates.
Project description:The Crown-of-Thorns starfish (COTS), Acanthaster planci, is a highly fecund predator of reef-building corals distributed throughout the Indo-Pacific. COTS population outbreaks cause substantial loss of coral cover, diminishing the integrity and resilience of the reef ecosystems thus increasing their susceptibility to climate change. We sequenced genomes of A. planci from the Great Barrier Reef, Australia (GBR) and Okinawa, Japan (OKI) to guide identification of species-specific peptide communication with potential applications in mitigation strategies. The genome-encoded proteins excreted and secreted into the surrounding seawater by COTS forming aggregations and by those escaping the predatory giant triton snail, Charonia tritonis, were identified LC-MS/MS.
Project description:Cell adhesion is tightly regulated by specific molecular interactions and detachment from the extracellular matrix modifies proliferation and survival. HAMLET (Human Alpha-lactalbumin Made LEthal to Tumor cells) is a protein-lipid complex with tumoricidal activity that also triggers tumor cell detachment in vitro and in vivo, suggesting that molecular interactions defining detachment are perturbed in cancer cells. To identify such interactions, cell membrane extracts were used in Far-western blots and HAMLET was shown to bind α-actinins; major F-actin cross-linking proteins and focal adhesion constituents. Synthetic peptide mapping revealed that HAMLET binds to the N-terminal actin-binding domain as well as the integrin-binding domain of α-actinin-4. By co-immunoprecipitation of extracts from HAMLET-treated cancer cells, an interaction with α-actinin-1 and -4 was observed. Inhibition of α-actinin-1 and α-actinin-4 expression by siRNA transfection increased detachment, while α-actinin-4-GFP over-expression significantly delayed rounding up and detachment of tumor cells in response to HAMLET. In response to HAMLET, adherent tumor cells rounded up and detached, suggesting a loss of the actin cytoskeletal organization. These changes were accompanied by a reduction in β1 integrin staining and a decrease in FAK and ERK1/2 phosphorylation, consistent with a disruption of integrin-dependent cell adhesion signaling. Detachment per se did not increase cell death during the 22 hour experimental period, regardless of α-actinin-4 and α-actinin-1 expression levels but adherent cells with low α-actinin levels showed increased death in response to HAMLET. The results suggest that the interaction between HAMLET and α-actinins promotes tumor cell detachment. As α-actinins also associate with signaling molecules, cytoplasmic domains of transmembrane receptors and ion channels, additional α-actinin-dependent mechanisms are discussed.