20 research outputs found
The Complete Genome Sequence of Fibrobacter succinogenes S85 Reveals a Cellulolytic and Metabolic Specialist
Fibrobacter succinogenes is an important member of the rumen
microbial community that converts plant biomass into nutrients usable by its
host. This bacterium, which is also one of only two cultivated species in its
phylum, is an efficient and prolific degrader of cellulose. Specifically, it has
a particularly high activity against crystalline cellulose that requires close
physical contact with this substrate. However, unlike other known cellulolytic
microbes, it does not degrade cellulose using a cellulosome or by producing high
extracellular titers of cellulase enzymes. To better understand the biology of
F. succinogenes, we sequenced the genome of the type strain
S85 to completion. A total of 3,085 open reading frames were predicted from its
3.84 Mbp genome. Analysis of sequences predicted to encode for
carbohydrate-degrading enzymes revealed an unusually high number of genes that
were classified into 49 different families of glycoside hydrolases, carbohydrate
binding modules (CBMs), carbohydrate esterases, and polysaccharide lyases. Of
the 31 identified cellulases, none contain CBMs in families 1, 2, and 3,
typically associated with crystalline cellulose degradation. Polysaccharide
hydrolysis and utilization assays showed that F. succinogenes
was able to hydrolyze a number of polysaccharides, but could only utilize the
hydrolytic products of cellulose. This suggests that F.
succinogenes uses its array of hemicellulose-degrading enzymes to
remove hemicelluloses to gain access to cellulose. This is reflected in its
genome, as F. succinogenes lacks many of the genes necessary to
transport and metabolize the hydrolytic products of non-cellulose
polysaccharides. The F. succinogenes genome reveals a bacterium
that specializes in cellulose as its sole energy source, and provides insight
into a novel strategy for cellulose degradation
Habilidades sociais: fator de proteção contra transtornos alimentares em adolescentes
Genome-wide association study of placental weight identifies distinct and shared genetic influences between placental and fetal growth
This is the final version. Available on open access from Nature Research via the DOI in this record. Data availability:
Individual cohorts contributing to the meta-analysis should be contacted directly as each cohort has different data access policies. GWAS summary statistics from this study are available via the EGG website (https://egg-consortium.org/placental-weight-2023.html, https://www.ebi.ac.uk/gwas/), as well as the GWAS catalog (https://www.ebi.ac.uk/gwas/, accession numbers GCST90275189, GCST90275190, GCST90275191, GCST90275192, GCST90275193, GCST90275194, GCST90275195, GCST90275196, GCST90275197, GCST90275198, GCST90275199). Access to personal-level information from Gen3G (including methylation array data) is subject to controlled access according to participants’ consent concerning sharing of personal data. Request for conditions of access and for data access should be addressed to Center Hospitalier Universitaire de Sherbrooke institutional ethics committee: [email protected] availability:
Analysis code is available from https://github.com/EarlyGrowthGenetics/placental_weight_codeA well-functioning placenta is essential for fetal and maternal health throughout pregnancy. Using placental weight as a proxy for placental growth, we report genome-wide association analyses in the fetal (n = 65,405), maternal (n = 61,228) and paternal (n = 52,392) genomes, yielding 40 independent association signals. Twenty-six signals are classified as fetal, four maternal and three fetal and maternal. A maternal parent-of-origin effect is seen near KCNQ1. Genetic correlation and colocalization analyses reveal overlap with birth weight genetics, but 12 loci are classified as predominantly or only affecting placental weight, with connections to placental development and morphology, and transport of antibodies and amino acids. Mendelian randomization analyses indicate that fetal genetically mediated higher placental weight is causally associated with preeclampsia risk and shorter gestational duration. Moreover, these analyses support the role of fetal insulin in regulating placental weight, providing a key link between fetal and placental growth.Wellcome Trus