https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51298 20%) during a reef-wide bleaching event in February 2020 at Heron Island on the Great Barrier Reef. We found that during this bleaching event, rates of NEP and NEC across replicate transects remained positive and did not change in response to bleaching. Repeated benthic surveys over a period of 20d indicated an increase in the percent area of bleached coral tissue, corroborated by relatively low Symbiodiniaceae densities (1/40.6×106cm-2) and dark-adapted photosynthetic yields in photosystem II of corals (1/40.5) sampled along each transect over this period. Given that a clear decline in coral health was not reflected in the overall NEC estimates, it is possible that elevated temperatures in the water column that compromise coral health enhanced the thermodynamic favorability for calcification in other ahermatypic benthic calcifiers. These data suggest that positive NEC on degraded reefs may not equate to the net positive accretion of a complex, three-dimensional reef structure in a future, warmer ocean. Critically, our study highlights that if coral cover continues to decline as predicted, NEC may no longer be an appropriate proxy for reef growth as the proportion of the NEC signal owed to ahermatypic calcification increases and coral dominance on the reef decreases.]]> Wed 30 Aug 2023 15:01:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25349 Wed 11 Apr 2018 16:07:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41216 Wed 07 Feb 2024 16:19:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38947 MTPAP/TENT6, encoding mitochondrial poly(A) polymerase (MTPAP), was first reported in six individuals of Old Order Amish descent demonstrating an early-onset, progressive spastic ataxia with optic atrophy and learning difficulties. MTPAP contributes to the regulation of mitochondrial gene expression through the polyadenylation of mitochondrially encoded mRNAs. Mitochondrial mRNAs with severely truncated poly(A) tails were observed in affected individuals, and mitochondrial protein expression was altered. Objective: To determine the genetic basis of a perinatal encephalopathy associated with stereotyped neuroimaging and infantile death in three patients from two unrelated families. Methods: Whole-exome sequencing was performed in two unrelated patients and the unaffected parents of one of these individuals. Variants and familial segregation were confirmed by Sanger sequencing. Polyadenylation of mitochondrial transcripts and de novo synthesis of mitochondrial proteins were assessed in patient's fibroblasts. Results: Compound heterozygous p.Ile428Thr and p.Arg523Trp substitutions in MTPAP were recorded in two affected siblings from one family, and a homozygous p.Ile385Phe missense variant identified in a further affected child from a second sibship. Mitochondrial poly(A) tail analysis demonstrated shorter posttranscriptional additions to the mitochondrial transcripts, as well as an altered expression of mitochondrial proteins in the fibroblasts of the two siblings compared with healthy controls. Conclusion: Mutations in MTPAP likely cause an autosomal recessive perinatal encephalopathy with lethality in the first year of life.]]> Fri 11 Mar 2022 12:45:18 AEDT ]]>