BUSCADOR RECOLECTA

Each .mat file, contains the following variables: - latitude/longitude: coastal point for the Mediterranean basin and islands within it; Dim = [7784,1] - elev_Rea, Hs_Rea: return levels computed for the present climate; Dim = [7784,1] - elev_Hist, elev_Rcp85, Hs_Hist, Hs_Rcp85: return levels computed for the historical asnd projected climate (from the 20 GCMs model used, see article); Dim = [7784,20], We provide return level data used for the assessement coastal hazards of Medicanes in the upcoming article "Coastal hazards of tropical-like cyclones over the Mediterranean Sea". For both significant wave height at 20m depth and coastal sea surface elevation, return levels are provided at 10 year (RLs_10year.mat) and 100 year (RLs_100year.mat) return periods., RLs_100year.mat; RLs_10year.mat, Peer reviewed

Numerical simulation results for the atmospheric Lamb waves generated by the Hunga-Tonga volcano explosion on January 15th 2022., Peer reviewed

7 pages. -- The file includes 7 figures. -- Figure S1. Selection of the combination of Hs and Tp values used in the 1D SWASH numerical simulations. The density plot represents the frequency that a combination of Hs and Tp is given in the intertropical areas ( 25 latitude, region where most of the coral reef islands are found) of the CFSR hindcast CAWCR Global wind-wave data set[1]. The black contour represents the area containing the maximum frequency and enclosing 90% of the Hs and Tp combinations. Taking advantage of previous experience, the 60 different combinations used for the simulations (black dots) has been chosen to include the most frequent combination as well as the extremes following lines of constant Hs Tp (dotted contour lines). -- Figure S2. Dependence of the wave setup with: a) significant wave height multiplied by peak period; b) sea level; c) reef length; d) island height; and e) Manning’s roughness coefficient. The central value of each box plot represents the median value, the lower (upper) limit of the box is the 25% (75%) quantile and the whiskers show the range of values between the 5% and 95% quantiles. -- Figure S3. Sensitivity tests for adjusted wave setup parameters in equation 3. Each parameter is randomly changed by up to 5% of its value and the rest are adjusted. Histograms represent the results of the process repeated 10000 times. -- Figure S4. Dependence of the flooding with sea level and island height for incoming waves with Hs = 4m and Tp = 20s, a reef length of 500 m and a Manning friction coefficient of 0.1. The colorplot is a bi-linear interpolation from the 36 values (black dots) obtained from the numerical simulations. The horizontal thick black line indicates the flooding that an island with 1.65 m would suffer with sea-level rise is no action is taken. The dashed black line indicates the evolution of the island height with sea-level rise if present-day flooding is required to remain constant. Thin black line indicate the isoline of a useddefine flooding threshold (in this case 0.1m3/s). The intersection between this line and the horizontal line (that shows the island height) indicates the sea level at which the user defined flooding threshold is over-passed. -- Figure S5. Same as Fig. 4 but with a Manning friction coefficient of 0.05. -- Figure S6. Number of island wave-induced flooded by more than 0.1m3/s with 0.5 m of mean sea level under different return periods and for different Manning friction coefficient. The total number of flooded islands for each return period is highly dependent on the Manning coefficient. -- Figure S7. Comparison between the flooding results from our simulations (Manning friction coefficient fixes to 0.1) with the flooding threshold derived by [2] (black dashed line in each panel). Note that we used different mean sea levels while keeping constant to 1 m the reef depth, whereas [2] changed their reef depth (Dree f ) and kept mean sea level as a constant value. Thus, to perform the comparison we computed the different reef depths as 1 m plus the corresponding mean sea level value. Consequently, our island height is transformed as the original island height minus the sea level to be consistent. Colours (in logarithmic colour scale) indicate the volume of flooding (in m3/s per linear meter of coastline). Our flooding values above the threshold are always below 0.01 m2/s., Peer reviewed

Return level data of extreme sea level and significant wave height (at 20m depth) for the Mediterranean basin and islands. 10, 20, 50, 100, and 200 years return period are provided for both variables. -- Each .mat file contains the following variables: - latitude/longitude: Dim = [111561,1] - RL_10, RL_20, RL_50, RL_100, RL_200: return levels; Dim = [111561,1], Return levels at 10, 20, 50, 100 and 200 years, for both coastal sea surface elevation and Hs variables., Peer reviewed

Return level data of extreme sea level and significant wave height (at 20m depth) for the Mediterranean basin and islands. 10, 20, 50, 100, and 200 years return period are provided for both variables. -- Each .mat file contains the following variables: - latitude/longitude: Dim = [111561,1] - RL_10, RL_20, RL_50, RL_100, RL_200: return levels; Dim = [111561,1], Return levels at 10, 20, 50, 100 and 200 years, for both coastal sea surface elevation and Hs variables., Peer reviewed

Muscle development is a multistep process that involves cell specification, myoblast fusion, myotube migration, and attachment to the tendons. In spite of great efforts trying to understand the basis of these events, little is known about the molecular mechanisms underlying myotube migration. Knowledge of the few molecular cues that guide this migration comes mainly from studies in Drosophila. The migratory process of Drosophila embryonic muscles involves a first phase of migration, where muscle progenitors migrate relative to each other, and a second phase, where myotubes migrate searching for their future attachment sites. During this phase, myotubes form extensive filopodia at their ends oriented preferentially toward their attachment sites. This myotube migration and the subsequent muscle attachment establishment are regulated by cell adhesion receptors, such as the conserved proteoglycan Kon-tiki/Perdido. Laminins have been shown to regulate the migratory behavior of many cell populations, but their role in myotube migration remains largely unexplored. Here, we show that laminins, previously implicated in muscle attachment, are indeed required for muscle migration to tendon cells. Furthermore, we find that laminins genetically interact with kon-tiki/perdido to control both myotube migration and attachment. All together, our results uncover a new role for the interaction between laminins and Kon-tiki/Perdido during Drosophila myogenesis. The identification of new players and molecular interactions underlying myotube migration broadens our understanding of muscle development and disease., Peer reviewed

Muscle development is a multistep process that involves cell specification, myoblast fusion, myotube migration, and attachment to the tendons. In spite of great efforts trying to understand the basis of these events, little is known about the molecular mechanisms underlying myotube migration. Knowledge of the few molecular cues that guide this migration comes mainly from studies in Drosophila. The migratory process of Drosophila embryonic muscles involves a first phase of migration, where muscle progenitors migrate relative to each other, and a second phase, where myotubes migrate searching for their future attachment sites. During this phase, myotubes form extensive filopodia at their ends oriented preferentially toward their attachment sites. This myotube migration and the subsequent muscle attachment establishment are regulated by cell adhesion receptors, such as the conserved proteoglycan Kon-tiki/Perdido. Laminins have been shown to regulate the migratory behavior of many cell populations, but their role in myotube migration remains largely unexplored. Here, we show that laminins, previously implicated in muscle attachment, are indeed required for muscle migration to tendon cells. Furthermore, we find that laminins genetically interact with kon-tiki/perdido to control both myotube migration and attachment. All together, our results uncover a new role for the interaction between laminins and Kon-tiki/Perdido during Drosophila myogenesis. The identification of new players and molecular interactions underlying myotube migration broadens our understanding of muscle development and disease., Peer reviewed

Muscle development is a multistep process that involves cell specification, myoblast fusion, myotube migration, and attachment to the tendons. In spite of great efforts trying to understand the basis of these events, little is known about the molecular mechanisms underlying myotube migration. Knowledge of the few molecular cues that guide this migration comes mainly from studies in Drosophila. The migratory process of Drosophila embryonic muscles involves a first phase of migration, where muscle progenitors migrate relative to each other, and a second phase, where myotubes migrate searching for their future attachment sites. During this phase, myotubes form extensive filopodia at their ends oriented preferentially toward their attachment sites. This myotube migration and the subsequent muscle attachment establishment are regulated by cell adhesion receptors, such as the conserved proteoglycan Kon-tiki/Perdido. Laminins have been shown to regulate the migratory behavior of many cell populations, but their role in myotube migration remains largely unexplored. Here, we show that laminins, previously implicated in muscle attachment, are indeed required for muscle migration to tendon cells. Furthermore, we find that laminins genetically interact with kon-tiki/perdido to control both myotube migration and attachment. All together, our results uncover a new role for the interaction between laminins and Kon-tiki/Perdido during Drosophila myogenesis. The identification of new players and molecular interactions underlying myotube migration broadens our understanding of muscle development and disease., Peer reviewed

Muscle development is a multistep process that involves cell specification, myoblast fusion, myotube migration, and attachment to the tendons. In spite of great efforts trying to understand the basis of these events, little is known about the molecular mechanisms underlying myotube migration. Knowledge of the few molecular cues that guide this migration comes mainly from studies in Drosophila. The migratory process of Drosophila embryonic muscles involves a first phase of migration, where muscle progenitors migrate relative to each other, and a second phase, where myotubes migrate searching for their future attachment sites. During this phase, myotubes form extensive filopodia at their ends oriented preferentially toward their attachment sites. This myotube migration and the subsequent muscle attachment establishment are regulated by cell adhesion receptors, such as the conserved proteoglycan Kon-tiki/Perdido. Laminins have been shown to regulate the migratory behavior of many cell populations, but their role in myotube migration remains largely unexplored. Here, we show that laminins, previously implicated in muscle attachment, are indeed required for muscle migration to tendon cells. Furthermore, we find that laminins genetically interact with kon-tiki/perdido to control both myotube migration and attachment. All together, our results uncover a new role for the interaction between laminins and Kon-tiki/Perdido during Drosophila myogenesis. The identification of new players and molecular interactions underlying myotube migration broadens our understanding of muscle development and disease., Peer reviewed

Additional file 1: Movie S1. Time-lapse movie of the system with F-actin forming and treadmilling in the grid., Ministerio de Ciencia, Innovación y Universidades. Ministerio de Ciencia, Innovación y Universidades, Peer reviewed