Farelo de gérmen de milho desengordurado na dieta de poedeiras comerciais de 28 a 44 semanas de idade Defatted corn germ meal in diets for laying hens from 28 to 44 weeks of age

Um experimento foi conduzido para avaliar os efeitos da inclusão de farelo de gérmen de milho desengordurado na dieta de galinhas de 28 a 44 semanas de idade. Foram utilizadas 240 poedeiras Hy-Line W36 distribuídas em delineamento inteiramente casualizado, com seis níveis de farelo de germen de milho desengordurado (0, 6, 12, 18, 24 e 30%),cada um com cinco repetições de oito aves. No período experimental, que durou quatro ciclos de 28 dias, foram avaliados os parâmetros de desempenho das aves (consumo de ração, produção de ovos, peso médio do ovo, massa de ovo e conversão alimentar) e de qualidade dos ovos (gravidade específica, índice de pigmentação da gema, porcentagem de gema e albúmen, porcentagem e espessura da casca e unidade haugh). Os níveis de farelo de gérmen de milho desengordurado tiveram efeito linear negativo sobre o consumo de ração e o índice de pigmentação da gema e efeito quadrático sobre a conversão alimentar. A inclusão de farelo de gérmen de milho desengordurado na dieta não influenciou as outras variáveis estudadas. O farelo de gérmen de milho desengordurado pode ser incluído em níveis de até 21,2% em rações para galinhas poedeiras.<br>This experiment was conducted to evaluate the effect of including defatted corn germ meal in diets for laying hens. It was assigned two hundred and forty laying hens to a randomized design, with six diets and five replicates of eight hens per diet. Experimental diets were formulated by inclusion of defatted corn germ meal at 0, 6, 12, 18, 24 and 30% level. The period experiment was carried out for four 28-day cycles and performance (feed intake, egg production, egg weight, egg mass and feed conversion) and the egg quality (egg specific gravity, yolk color, yolk and albumen percentages, shell percentages, shell thickness and Haugh unity) were the evaluated parameters. Negative linear effect was observed for feed intake and yolk pigmentation by increasingly including defatted corn germ meal in diets for laying hens. Quadratic effect of defatted corn germ meal for feed conversion was also observed. No statistical differences were observed for any other parameters. Defatted corn germ meal can be included at 21.2% in laying hens diets

HNRNPC haploinsufficiency affects alternative splicing of intellectual disability-associated genes and causes a neurodevelopmental disorder

Heterogeneous nuclear ribonucleoprotein C (HNRNPC) is an essential, ubiquitously abundant protein involved in mRNA processing. Genetic variants in other members of the HNRNP family have been associated with neurodevelopmental disorders. Here, we describe 13 individuals with global developmental delay, intellectual disability, behavioral abnormalities, and subtle facial dysmorphology with heterozygous HNRNPC germline variants. Five of them bear an identical in-frame deletion of nine amino acids in the extreme C terminus. To study the effect of this recurrent variant as well as HNRNPC haploinsufficiency, we used induced pluripotent stem cells (iPSCs) and fibroblasts obtained from affected individuals. While protein localization and oligomerization were unaffected by the recurrent C-terminal deletion variant, total HNRNPC levels were decreased. Previously, reduced HNRNPC levels have been associated with changes in alternative splicing. Therefore, we performed a meta-analysis on published RNA-seq datasets of three different cell lines to identify a ubiquitous HNRNPC-dependent signature of alternative spliced exons. The identified signature was not only confirmed in fibroblasts obtained from an affected individual but also showed a significant enrichment for genes associated with intellectual disability. Hence, we assessed the effect of decreased and increased levels of HNRNPC on neuronal arborization and neuronal migration and found that either condition affects neuronal function. Taken together, our data indicate that HNRNPC haploinsufficiency affects alternative splicing of multiple intellectual disability-associated genes and that the developing brain is sensitive to aberrant levels of HNRNPC. Hence, our data strongly support the inclusion of HNRNPC to the family of HNRNP-related neurodevelopmental disorders

HNRNPC haploinsufficiency affects alternative splicing of intellectual disability-associated genes and causes a neurodevelopmental disorder

Heterogeneous nuclear ribonucleoprotein C (HNRNPC) is an essential, ubiquitously abundant protein involved in mRNA processing. Genetic variants in other members of the HNRNP family have been associated with neurodevelopmental disorders. Here, we describe 13 individuals with global developmental delay, intellectual disability, behavioral abnormalities, and subtle facial dysmorphology with heterozygous HNRNPC germline variants. Five of them bear an identical in-frame deletion of nine amino acids in the extreme C terminus. To study the effect of this recurrent variant as well as HNRNPC haploinsufficiency, we used induced pluripotent stem cells (iPSCs) and fibroblasts obtained from affected individuals. While protein localization and oligomerization were unaffected by the recurrent C-terminal deletion variant, total HNRNPC levels were decreased. Previously, reduced HNRNPC levels have been associated with changes in alternative splicing. Therefore, we performed a meta-analysis on published RNA-seq datasets of three different cell lines to identify a ubiquitous HNRNPC-dependent signature of alternative spliced exons. The identified signature was not only confirmed in fibroblasts obtained from an affected individual but also showed a significant enrichment for genes associated with intellectual disability. Hence, we assessed the effect of decreased and increased levels of HNRNPC on neuronal arborization and neuronal migration and found that either condition affects neuronal function. Taken together, our data indicate that HNRNPC haploinsufficiency affects alternative splicing of multiple intellectual disability-associated genes and that the developing brain is sensitive to aberrant levels of HNRNPC. Hence, our data strongly support the inclusion of HNRNPC to the family of HNRNP-related neurodevelopmental disorders. [Display omitted] We identified genetic variants of HNRNPC in 13 individuals with intellectual disability and global developmental delay. Through a meta-analysis of multiple cell types, we found that loss of HNRNPC affects alternative splicing, in particular of intellectual disability-associated genes. In vivo assays confirmed that neurodevelopment was affected by aberrant HNRNPC levels