Data from: A statistical framework to explore ontogenetic growth variation among individuals and populations: a marine fish example

Growth is a fundamental biological process, driven by a multitude of intrinsic (within-individual) and extrinsic (environmental) factors, that underpins individual fitness and population demographics. Focussing on the comprehensive information stored in aquatic and terrestrial organism hard parts, we develop a series of increasingly complex hierarchical models to explore spatial and temporal sources of growth variation, ranging in resolution from within individuals to across a species. We apply this modelling framework to an extensive data set of otolith increment measurements from tiger flathead (Platycephalus richardsoni), a demersal commercially exploited fish that inhabits the warming waters of south-east Australia. We recreated growth histories (biochronology) up to four decades in length from seven fishing areas spanning this species' range. The dominant pattern in annual growth was an age-dependent, allometric decline that varied amongst individuals, sexes, fishing areas, years and cohorts. We found evidence for among-area differences in growth rate selectivity whereby younger fish at capture were generally faster growers. Temporal growth variation was partitioned into two main sources: extrinsic year-to-year annual fluctuations in environmental conditions and persistent cohort-specific growth differences, reflecting density dependence and/or juvenile experience. Despite low levels of among-individual growth synchrony within areas, we detected a regionally coherent signal of increasing average growth rate through time, a trend related to oceanic warming. At the southerly (poleward) range limit, growth was only weakly related to temperature, but further north in warmer waters this relationship strengthened until at the species' equatorward range limit, growth declined with increasing temperatures. We partitioned these species-wide and area-specific phenotypic responses into within and among-individual components using a reaction norm approach. Individual tiger flathead likely possess sufficient growth plasticity to successfully adapt to warming waters across much of their range, but increased future warming in the north will continue to depress growth, affecting individual fitness and even population persistence. Our modelling framework is directly applicable to other long-term, individual-based, data sets such as those derived from tree rings, corals, and tag-recapture studies, and provides an unprecedented level of resolution into the drivers of growth variation and the ecological and evolutionary implications of environmental and climatic change

tiger flathead biochronologies

Sheet 1: Estimated annual average growth tiger flathead for each fishing area (figure 4a-g & figure 5). Sheet 2: estimated cohort specific growth for each fishing area (figure 4h-n). Year: 1 Jan – 31 Dec. Area: fishing area (see figure 1). Bottomtemp: annual average bottom temperature (oC) for each fishing area. See appendix B for methodological details. annualgrowth: estimate of annual average growth (in mm) derived from model BLUPs. cohortgrowth: estimate of cohort-specific growth (in mm) derived from model BLUPs. SE: standard error

environmental data

Environmental covariates used in the analysis of inter-annual growth variation. Year: 1 Jan – 31 Dec. Area: fishing area (see figure 1). Centlat: central latitude of fishing area. Centlong: central longitude of fishing area. Bottomtemp: annual average bottom temperature (oC) for each fishing area based on SynTS and HadISST data sets. See appendix B for methodological details. CPUE: annual average catch per unit effort (CPUE) for each fishing area. See appendix B for methodological details

increment averages

Table of otolith increment measurements averaged by age and year for each fishing area. Area: fishing area. Year: 1 Jan – 31 Dec. Age1- Age18: fish ages

incrmement measurements

Raw increment measurements and biological data for 4318 (of 6143) fish from fishing areas EBS and ETAS. This subset represents ~74% of increment data used in analyses. The full data set has not been published as it underpins commercially sensitive stock assessments and is held by CSIRO in confidence on behalf of AFMA. Requests for the full data set will be considered on a case by case basis and must be directed to Dr David Smith, Research Director Marine Resources & Industries, CSIRO Oceans & Atmosphere Flagship. David(dot)C(dot)Smith(at)csiro(dot)au. Area: fishing area; FishID: unique identifier for each individual; Sex: M or F; Gear:otter trawl (OT), Danish seine (DS) or unknown; Capyear: capture year; Capmonth: capture month; Floorlength: fish length (cm) rounded down to the nearest whole number; AdjAge: adjusted fish age, based on increment count, otolith edge type, date of capture and the species’ nominal birthday (1 Jan). This is the age-at-capture variable in the paper, and is a fish’s age in whole years; DeciAge: decimal age based on date of capture in relation to birth date; Radius: otolith radius along measuring transect in mm; YOB: year of birth, or year class. Year: calendar year in which a given increment was deposited; Age: age in years corresponding to a given increment; Increment: width of otolith annuli in m

Deletion of the Protein Kinase A/Protein Kinase G Target SMTNL1 Promotes an Exercise-adapted Phenotype in Vascular Smooth Muscle*S⃞

In vivo protein kinases A and G (PKA and PKG) coordinately phosphorylate a broad range of substrates to mediate their various physiological effects. The functions of many of these substrates have yet to be defined genetically. Herein we show a role for smoothelin-like protein 1 (SMTNL1), a novel in vivo target of PKG/PKA, in mediating vascular adaptations to exercise. Aortas from smtnl1-/- mice exhibited strikingly enhanced vasorelaxation before exercise, similar in extent to that achieved after endurance training of wild-type littermates. Additionally, contractile responses to α-adrenergic agonists were greatly attenuated. Immunological studies showed SMTNL1 is expressed in smooth muscle and type 2a striated muscle fibers. Consistent with a role in adaptations to exercise, smtnl1-/- mice also exhibited increased type 2a fibers before training and better performance after forced endurance training compared smtnl1+/+ mice. Furthermore, exercise was found to reduce expression of SMTNL1, particularly in female mice. In both muscle types, SMTNL1 is phosphorylated at Ser-301 in response to adrenergic signals. In vitro SMTNL1 suppresses myosin phosphatase activity through a substrate-directed effect, which is relieved by Ser-301 phosphorylation. Our findings suggest roles for SMTNL1 in cGMP/cAMP-mediated adaptations to exercise through mechanisms involving direct modulation of contractile activity

Deletion of the Protein Kinase A/Protein Kinase G Target SMTNL1 Promotes an Exercise-adapted Phenotype in Vascular Smooth Muscle

In vivo protein kinases A and G (PKA and PKG) coordinately phosphorylate a broad range of substrates to mediate their various physiological effects. The functions of many of these substrates have yet to be defined genetically. Herein we show a role for smoothelin-like protein 1 (SMTNL1) a novel in vivo target of PKG/PKA in mediating vascular adaptations to exercise. Aortas from smtnl1-/- mice exhibited strikingly enhanced vasorelaxation before exercise similar in extent to that achieved after endurance training of wild-type littermates. Additionally con- tractile responses to alpha-adrenergic agonists were greatly attenuated. Immunological studies showed SMTNL1 is expressed in smooth muscle and type 2a striated muscle fibers. Consistent with a role in adaptations to exercise smtnl1-/- mice also exhibited increased type 2a fibers before training and better performance after forced endurance training compared smtnl1+/+ mice. Furthermore exercise was found to reduce expression of SMTNL1 particularly in female mice. In both muscle types SMTNL1 is phosphorylated at Ser-301 in response to adrenergic signals. In vitro SMTNL1 suppresses myosin phosphatase activity through a substrate-directed effect which is relieved by Ser- 301 phosphorylation. Our findings suggest roles for SMTNL1 in cGMP/cAMP-mediated adaptations to exercise through mechanisms involving direct modulation of contractile activity. Originally published Journal of Biological Chemistry Vol. 283 No. 17 Apr 200