Sex-linked Dwarf Research Articles

Growth hormone receptor gene influences mitochondrial function and chicken lipid metabolism by AMPK-PGC1\u03b1-PPAR signaling pathway

BackgroundAdipose tissue is an important endocrine and energy-storage organ in organisms, and it plays a crucial role in the energy-metabolism balance. Previous studies have found that sex-linked dwarf (SLD) chickens generally have excessively high abdominal fat deposition during the growing period, which increases feeding costs. However, the underlying mechanism of this fat deposition during the growth of SLD chickens remains unknown.ResultsThe Oil Red O staining showed that the lipid-droplet area of SLD chickens was larger than that of normal chickens in E15 and 14d. Consistently, TG content in the livers of SLD chickens was higher than that of normal chickens in E15 and 14d. Further, lower ΔΨm and lower ATP levels and higher MDA levels were observed in SLD chickens than normal chickens in both E15 and 14d. We also found that overexpression of GHR reduced the expression of genes related to lipid metabolism (AMPK, PGC1α, PPARγ, FAS, C/EBP) and oxidative phosphorylation (CYTB, CYTC, COX1, ATP), as well as reducing ΔΨm and ATP levels and increasing MDA levels. In addition, overexpression of GHR inhibited fat deposition in CPPAs, as measured by Oil Red O staining. On the contrary, knockdown of GHR had the opposite effects in vitro.ConclusionsIn summary, we demonstrate that GHR promotes mitochondrial function and inhibits lipid peroxidation as well as fat deposition in vivo and in vitro. Therefore, GHR is essential for maintaining the stability of lipid metabolism and regulating mitochondrial function in chicken.

Growth Hormone Receptor Controls Adipogenic Differentiation of Chicken Bone Marrow Mesenchymal Stem Cells by Affecting Mitochondrial Biogenesis and Mitochondrial Function.

Growth hormone receptor (GHR) can activate several signaling pathways after binding to growth hormone (GH) to regulate cell growth and development. Sex-linked dwarf (SLD) chickens, normal protein functions are prevented because of exon mutations in the GHR gene, have more severe fat deposition. However, the specific molecular mechanisms responsible for this phenotype remains unclear. We therefore investigated the effect of the GHR gene on adipogenic differentiation of chicken bone marrow mesenchymal stem cells (BMSCs). We found that bone marrow fat deposition was more severe in SLD chickens compared to normal chickens, and the expression of genes related to adipogenic differentiation was enhanced in SLD chicken BMSCs. We also detected enhanced mitochondrial function of BMSCs in SLD chickens. In vitro, overexpression of GHR in chicken BMSCs increased mitochondrial membrane potential but decreased reactive oxygen and ATP contents, oxidative phosphorylation complex enzyme activity, and mitochondrial number. Expression of genes associated with mitochondrial biogenesis and function was repressed during adipogenic differentiation in chicken BMSCs, the adipogenic differentiation capacity of chicken BMSCs was also repressed. With knockdown of GHR, opposite results were observed. We concluded that GHR inhibited adipogenic differentiation of chicken BMSCs by suppressing mitochondrial biogenesis and mitochondrial function.

The impact of sex-linked dwarf gene on hormonal reproductive profiles and biochemical traits in Iraqi dwarf roosters

The current experiment was aimed to explore the influencing of the sex-linked dwarf gene on some fertility hormones and biochemical profile in normal local and dwarf roosters. Thirty normal local and dwarf roosters at age 28 weeks were housed at opened system for 6 weeks. At end of 6th week, blood samples collected from all roosters and centrifuged to obtained sera for measuring the concentrations of Interstitial cell stimulating hormone ‘ICSH’, Follicle stimulating hormone ‘FSH’ and testosterone hormone, total protein, albumen, globulin, glutamic oxaloacetic transaminase ‘GOT’, Alkaline phosphatase ‘ALP’, and glutamic pyruvic transaminase ‘GPT’. The statistical analysis documented significant (P<0.05) decline in FSH and testosterone hormone in dwarf group roosters compared with normal local roosters. As well as, the level of total protein and globulin registered significant decline (P<0.05) in dwarf group roosters in comparison with normal local group roosters. On the other hand, the level of hepatic enzymes, GOT, GPT and ALK, recorded a significant (P<0.05) elevation in dwarf group roosters when compared with normal local group roosters. Concluded, that the sex-linked dwarf gene could be affected on hormonal fecundity profile and some biochemical traits in dwarf roosters.

High expression of BCL6 inhibits the differentiation and development of hematopoietic stem cells and affects the growth and development of chickens

BackgroundB-cell CLL/lymphoma 6 (BCL6) is a transcriptional master regulator that represses more than 1200 potential target genes. Our previous study showed that a decline in blood production in runting and stunting syndrome (RSS) affected sex-linked dwarf (SLD) chickens compared to SLD chickens. However, the association between BCL6 gene and hematopoietic function remains unknown in chickens.MethodsIn this study, we used RSS affected SLD (RSS-SLD) chickens, SLD chickens and normal chickens as research object and overexpression of BCL6 in hematopoietic stem cells (HSCs), to investigate the effect of the BCL6 on differentiation and development of HSCs.ResultsThe results showed that comparison of RSS-SLD chickens with SLD chickens, the BCL6 was highly expressed in RSS-SLD chickens bone marrow. The bone marrow of RSS-SLD chickens was exhausted and red bone marrow was largely replaced by yellow bone marrow, bone density was reduced, and the levels of immature erythrocytes in peripheral blood were increased. At the same time, the hematopoietic function of HSCs decreased in RSS-SLD chickens, which was manifested by a decrease in the hematopoietic growth factors (HGFs) EPO, SCF, TPO, and IL-3, as well as hemoglobin α1 and hemoglobin β expression. Moreover, mitochondrial function in the HSCs of RSS-SLD chickens was damaged, including an increase in ROS production, decrease in ATP concentration, and decrease in mitochondrial membrane potential (ΔΨm). The same results were also observed in SLD chickens compared with normal chickens; however, the symptoms were more serious in RSS-SLD chickens. Additionally, after overexpression of the BCL6 in primary HSCs, the secretion of HGFs (EPO, SCF, TPO and IL-3) was inhibited and the expression of hemoglobin α1 and hemoglobin β was decreased. However, cell proliferation was accelerated, apoptosis was inhibited, and the HSCs entered a cancerous state. The function of mitochondria was also abnormal, ROS production was decreased, and ATP concentration and ΔΨm were increased, which was related to the inhibition of apoptosis of stem cells.ConclusionsTaken together, we conclude that the high expression of BCL6 inhibits the differentiation and development of HSCs by affecting mitochondrial function, resulting in impaired growth and development of chickens. Moreover, the abnormal expression of BCL6 might be a cause of the clinical manifestations of chicken comb, pale skin, stunted growth and development, and the tendency to appear RSS in SLD chickens.

Integrative Analyses of mRNA Expression Profile Reveal SOCS2 and CISH Play Important Roles in GHR Mutation-Induced Excessive Abdominal Fat Deposition in the Sex-Linked Dwarf Chicken.

Sex-linked dwarf (SLD) chicken, which is caused by a recessive mutation of the growth hormone receptor (GHR), has been widely used in the Chinese broiler industry. However, it has been found that the SLD chicken has more abdominal fat deposition than normal chicken. Excessive fat deposition not only reduced the carcass quality of the broilers but also reduced the immunity of broilers to diseases. To find out the key genes and the precise regulatory pathways that were involved in the GHR mutation-induced excessive fat deposition, we used high-fat diet (HFD) and normal diet to feed the SLD chicken and normal chicken and analyzed the differentially expressed genes (DEGs) among the four groups. Results showed that the SLD chicken had more abdominal fat deposition and larger adipocytes size than normal chicken and HFD can promote abdominal fat deposition and induce adipocyte hypertrophy. RNA sequencing results of the livers and abdominal fats from the above chickens revealed that many DEGs between the SLD and normal chickens were enriched in fat metabolic pathways, such as peroxisome proliferator-activated receptor (PPAR) signaling, extracellular matrix (ECM)-receptor pathway, and fatty acid metabolism. Importantly, by constructing and analyzing the GHR-downstream regulatory network, we found that suppressor of cytokine signaling 2 (SOCS2) and cytokine-inducible SH2-containing protein (CISH) may involve in the GHR mutation-induced abdominal fat deposition in chicken. The ectopic expression of SOCS2 and CISH in liver-related cell line leghorn strain M chicken hepatoma (LMH) cell and immortalized chicken preadipocytes (ICP) revealed that these two genes can regulate fatty acid metabolism, adipocyte differentiation, and lipid droplet accumulation. Notably, overexpression of SOCS2 and CISH can rescue the hyperactive lipid metabolism and excessive lipid droplet accumulation of primary liver cell and preadipocytes that were isolated from the SLD chicken. This study found some genes and pathways involved in abdominal fat deposition of the SLD chicken and reveals that SOCS2 and CISH are two key genes involved in the GHR mutation-induced excessive fat deposition of the SLD chicken.

Mutation of TWNK Gene Is One of the Reasons of Runting and Stunting Syndrome Characterized by mtDNA Depletion in Sex-Linked Dwarf Chicken.

Runting and stunting syndrome (RSS), which is characterized by low body weight, generally occurs early in life and leads to considerable economic losses in the commercial broiler industry. Our previous study has suggested that RSS is associated with mitochondria dysfunction in sex-linked dwarf (SLD) chickens. However, the molecular mechanism of RSS remains unknown. Based on the molecular diagnostics of mitochondrial diseases, we identified a recessive mutation c. 409G > A (p. Ala137Thr) of Twinkle mitochondrial DNA helicase (TWNK) gene and mitochondrial DNA (mtDNA) depletion in RSS chickens’ livers from strain N301. Bioinformatics investigations supported the pathogenicity of the TWNK mutation that is located on the extended peptide linker of Twinkle primase domain and might further lead to mtDNA depletion in chicken. Furthermore, overexpression of wild-type TWNK increases mtDNA copy number, whereas overexpression of TWNK A137T causes mtDNA depletion in vitro. Additionally, the TWNK c. 409G > A mutation showed significant associations with body weight, daily gain, pectoralis weight, crureus weight, and abdominal fat weight. Taken together, we corroborated that the recessive TWNK c. 409G > A (p. Ala137Thr) mutation is associated with RSS characterized by mtDNA depletion in SLD chicken.

Runting and Stunting Syndrome Is Associated With Mitochondrial Dysfunction in Sex-Linked Dwarf Chicken.

Runting and stunting syndrome (RSS) in chicken are commonly known as “frozen chicken.” The disease is characterized by lower body weight and slow growth and the incidence rate is widely 5%–20% in sex-linked dwarf (SLD) chickens. However, the etiology of RSS in chickens has plagued researchers for several decades. In this study, histopathology studies demonstrated that the hepatocytes of the RSS chickens contain many mitochondria with damaged and outer and inner membrane along with vacuolar hydropic degeneration. No mtDNA mutation was detected, but our microarray data showed that RSS chickens exhibited abnormal expression of genes, many of which are involved in oxidative phosphorylation (OXPHOS) and fatty acid metabolism. In particular, nuclear gene IGF2BP3 was upregulated in RSS chickens' liver cells. The abnormal expression of these genes is likely to impair the OXPHOS, resulting in reduced ATP synthesis in the hepatocytes of the RSS chickens, which may in turn leads to poor weight gain and retarded growth or stunting of chicks. Our findings suggest that mitochondria dysfunction rather than chronic inflammation is responsible for the reduced growth and RSS in SLD chickens. Mutations in GHR have been shown to compromise mitochondrial function in SLD chickens. Since the mitochondrial damage in the RSS chicken is more severe, we suggest that extra genes are likely to be affected to exacerbate the phenotype.

Growth Hormone Receptor Gene is Essential for Chicken Mitochondrial Function In Vivo and In Vitro.

The growth hormone receptor (GHR) gene is correlated with many phenotypic and physiological alternations in chicken, such as shorter shanks, lower body weight and muscle mass loss. However, the role of the GHR gene in mitochondrial function remains unknown in poultry. In this study, we assessed the function of mitochondria in sex-linked dwarf (SLD) chicken skeletal muscle and interfered with the expression of GHR in DF-1 cells to investigate the role of the GHR gene in chicken mitochondrial function both in vivo and in vitro. We found that the expression of key regulators of mitochondrial biogenesis and mitochondrial DNA (mtDNA)-encoded oxidative phosphorylation (OXPHOS) genes were downregulated and accompanied by reduced enzymatic activity of OXPHOS complexes in SLD chicken skeletal muscle and GHR knockdown cells. Then, we assessed mitochondrial function by measuring mitochondrial membrane potential (ΔΨm), mitochondrial swelling, reactive oxygen species (ROS) production, malondialdehyde (MDA) levels, ATP levels and the mitochondrial respiratory control ratio (RCR), and found that mitochondrial function was impaired in SLD chicken skeletal muscle and GHR knockdown cells. In addition, we also studied the morphology and structure of mitochondria in GHR knockdown cells by transmission electron microscopy (TEM) and MitoTracker staining. We found that knockdown of GHR could reduce mitochondrial number and alter mitochondrial structure in DF-1 cells. Above all, we demonstrated for the first time that the GHR gene is essential for chicken mitochondrial function in vivo and in vitro.

Let-7b Regulates Myoblast Proliferation by Inhibiting IGF2BP3 Expression in Dwarf and Normal Chicken.

The sex-linked dwarf chicken is caused by the mutation of growth hormone receptor (GHR) gene and characterized by shorter shanks, lower body weight, smaller muscle fiber diameter and fewer muscle fiber number. However, the precise regulatory pathways that lead to the inhibition of skeletal muscle growth in dwarf chickens still remain unclear. Here we found a let-7b mediated pathway might play important role in the regulation of dwarf chicken skeletal muscle growth. Let-7b has higher expression in the skeletal muscle of dwarf chicken than in normal chicken, and the expression of insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3), which is a translational activator of IGF2, showed opposite expression trend to let-7b. In vitro cellular assays validated that let-7b directly inhibits IGF2BP3 expression through binding to its 3′UTR region, and the protein level but not mRNA level of IGF2 would be reduced in let-7b overexpressed chicken myoblast. Let-7b can inhibit cell proliferation and induce cell cycle arrest in chicken myoblast through let-7b-IGF2BP3-IGF2 signaling pathway. Additionally, let-7b can also regulate skeletal muscle growth through let-7b-GHR-GHR downstream genes pathway, but this pathway is non-existent in dwarf chicken because of the deletion mutation of GHR 3′UTR. Notably, as the loss binding site of GHR for let-7b, let-7b has enhanced its binding and inhibition on IGF2BP3 in dwarf myoblast, suggesting that the miRNA can balance its inhibiting effect through dynamic regulate its binding to target genes. Collectively, these results not only indicate that let-7b can inhibit skeletal muscle growth through let-7b-IGF2BP3-IGF2 signaling pathway, but also show that let-7b regulates myoblast proliferation by inhibiting IGF2BP3 expression in dwarf and normal chickens.

P3005 Genome-wide transcriptomic analysis of liver in sex-linked dwarf and wild-type chickens

P3005 Genome-wide transcriptomic analysis of liver in sex-linked dwarf and wild-type chickens

Integrative Analyses of miRNA-mRNA Interactions Reveal let-7b, miR-128 and MAPK Pathway Involvement in Muscle Mass Loss in Sex-Linked Dwarf Chickens.

The sex-linked dwarf (SLD) chicken is an ideal model system for understanding growth hormone (GH)-action and growth hormone receptor (GHR) function because of its recessive mutation in the GHR gene. Skeletal muscle mass is reduced in the SLD chicken with a smaller muscle fiber diameter. Our previous study has presented the mRNA and miRNA expression profiles of the SLD chicken and normal chicken between embryo day 14 and seven weeks of age. However, the molecular mechanism of GHR-deficient induced muscle mass loss is still unclear, and the key molecules and pathways underlying the GHR-deficient induced muscle mass loss also remain to be illustrated. Here, by functional network analysis of the differentially expressed miRNAs and mRNAs between the SLD and normal chickens, we revealed that let-7b, miR-128 and the MAPK pathway might play key roles in the GHR-deficient induced muscle mass loss, and that the reduced cell division and growth are potential cellular processes during the SLD chicken skeletal muscle development. Additionally, we also found some genes and miRNAs involved in chicken skeletal muscle development, through the MAPK, PI3K-Akt, Wnt and Insulin signaling pathways. This study provides new insights into the molecular mechanism underlying muscle mass loss in the SLD chickens, and some regulatory networks that are crucial for chicken skeletal muscle development.

Pattern of GHR mRNA expression and body growth in the S2 line of sex-linked dwarf chickens

Sex-linked dwarf (SLD) chickens have been widely used in cross breeding of broilers and laying hens. To study the molecular mechanisms underlying growth hormone receptor (GHR) in SLD chickens, the expression profiles of GHR were measured in three growth related tissues (liver, breast, and thigh) in male and female S2 SLD chickens at seven growth stages (1 day, 3 weeks, 7 weeks, 9 weeks, 11 weeks, 13 weeks, and 15 weeks). Growth curves of body weight were fitted using logistic and Gompertz models. The results show that the inflexion week and inflexion weight in male chickens was earlier than in female chickens. Regarding the expression profiles of GHR, there was no significant difference between tissues at hatching. The expression peaked at 7 weeks and dropped by degrees in muscle tissue; hepatic expression increased with age and was positively correlated with body weight. Taken together, these results would provide a basis for further study on the molecular mechanisms underlying GHR regulation in SLD chickens.

Effect of sex-linked dwarf gene on exterior appearance, productive performance and egg characteristics in a colored broiler dam line

The effect of sex-linked dwarf gene was investigated through comparison of dwarf hens with their full-sib normal sisters obtained by mating heterozygous males (DW/dw) to normal females (DW/_) from line F (used as maternal form for production of slow-growing colored chickens) with respect to the following traits: body weight, shank and keel length at 40 weeks of age, age of sexual maturity (at 50 % production), egg production, egg weight, feed intake, feed utilization, livability, fertility, hatchability and egg quality characteristics. The results demonstrated that the dw gene caused statistically significant reduction of body weight by 29.15 %, shank length by 20.17 %, keel length by 7 % and egg weight by 5.72 % (p&lt;0.001). The hens with normal genotype attained sexual maturity 7 days earlier (p&lt;0.001), but nevertheless, rate of lay was similar to that of mini forms. There were no considerable differences between both genetic groups with respect to livability percentage over the production cycle. Dwarf hens consumed by 23.38 % less feed (p&lt;0.01) than normal sized hens and converted nutrients more efficiently by 12.69 % (p&lt;0.05). The presence of dw gene in hen genotype increased the eggshell percentage, reduced egg yolk and albumen weights and had no effect on their quality. The positive effect of the sex-linked dwarf gene on economically important traits - feed intake and feed conversion, hatchability of eggs set, is a prerequisite for the development of more efficient broiler breeder hens for production of slow-growing chickens.

MicroRNAs expression profiles in adipose tissues and liver from sex-linked dwarf and normal chickens.

MicroRNAs expression profiles in adipose tissues and liver from sex-linked dwarf and normal chickens.

Analysis of differentially expressed genes and signaling pathways related to intramuscular fat deposition in skeletal muscle of sex-linked dwarf chickens.

Intramuscular fat (IMF) plays an important role in meat quality. However, the molecular mechanisms underlying IMF deposition in skeletal muscle have not been addressed for the sex-linked dwarf (SLD) chicken. In this study, potential candidate genes and signaling pathways related to IMF deposition in chicken leg muscle tissue were characterized using gene expression profiling of both 7-week-old SLD and normal chickens. A total of 173 differentially expressed genes (DEGs) were identified between the two breeds. Subsequently, 6 DEGs related to lipid metabolism or muscle development were verified in each breed based on gene ontology (GO) analysis. In addition, KEGG pathway analysis of DEGs indicated that some of them (GHR, SOCS3, and IGF2BP3) participate in adipocytokine and insulin signaling pathways. To investigate the role of the above signaling pathways in IMF deposition, the gene expression of pathway factors and other downstream genes were measured by using qRT-PCR and Western blot analyses. Collectively, the results identified potential candidate genes related to IMF deposition and suggested that IMF deposition in skeletal muscle of SLD chicken is regulated partially by pathways of adipocytokine and insulin and other downstream signaling pathways (TGF-β/SMAD3 and Wnt/catenin-β pathway).

Assessing the thermo-tolerance potentials of five commercial layer chicken genotypes under long-term heat stress environment as measured by their performance traits

This study was conducted to test the thermo-tolerance ability of five commercial chicken genotypes (Lohmann Brown, LB; Lohmann White, LW; New Hampshire, NH; White Leghorn selected for low feed expenditure, WL-FE and White Leghorn with sex-linked dwarf gene, WL-dw) under long-term heat exposure. Two-hundred forty female chickens were assigned to a completely randomized design in a 5 × 2 factorial arrangements (five genetic groups and two ambient temperatures [thermo-neutral, 18–20 °C; heat stress, 30–32 °C]). Individual eggs were collected on daily basis while egg weight and feed intake were determined on individual and group basis at 28-days intervals, respectively. Shell quality traits were determined at 25, 40 and 56 weeks age. No Genotype × ambient temperature interactions were found except for body weight and egg deformation. Chickens at thermo-neutral temperature produced significantly heavier eggs than those of heat-exposed (60 g vs. 54 g). Hen-housed egg production of chickens in thermo-neutral temperature was significantly higher than those of heat-stressed (76.8 % vs. 66.2 %). Daily egg mass production at thermo-neutral and heat stressed chickens was 46 g and 35.8 g, respectively. Feed consumption in heat-stressed and thermo-neutral chickens was 109 and 80.8 g, respectively. Shell thickness, breaking strength and Haugh unit values were significantly reduced in heat-stressed chickens. Among heat-exposed chickens, the NH had the highest body weight while the LW produced 10 % more eggs than the group average. The heat-induced effect on shell quality traits was lowest in LW chickens. The results indicated that the magnitude of heat stress was breed dependent in which the LB showed poor adaptability to heat stress while both NH and LW genotypes demonstrated better thermo-tolerance ability.

A Rapid and Cost Effective Method for Genotyping Two Types of GHR Mutations in Sex-Linked Dwarf Chicken

A Rapid and Cost Effective Method for Genotyping Two Types of GHR Mutations in Sex-Linked Dwarf Chicken

The Effects of Different Sex-Linked Dwarf Variations on Chinese Native Chickens

Variants in chicken growth hormone receptor (GHR) gene lead to sex-linked dwarf (SLD) chickens, but effects of different variants are distinct. In this study, 11 SLD chicken breeds or strains including 3 Chinese native breeds and 8 breeding strains were studied in order to investigate the effects of different sex-linked dwarf variations on growth performance. The results showed that there were three reasons which could lead to dwarfism in the 11 breeds or strains. Firstly, an about 1.7 kb deletion of growth hormone receptor (GHR) gene leads to dwarfism in Jiangxi dwarf chicken, strains GF24, GF26, N308, N309, and N310. Secondly, a T354C mutation in exon 5 of the GHR gene leads to dwarfism in strains N301 and N305. Thirdly, an unknown variant leads to dwarfism in Guizhou Yellow Dwarf chicken and Yixing Bantam chicken. In addition, all individuals of N303 had the 1.7 kb deletion of the GHR gene, and additionally, some of them also carried the T354C mutation. As far as the performance of individuals were compared among T354C homozygote, deletion homozygote, and heterozygote carrying both T354C and deletion, it was found that the T354C's impacts on body weight of Chinese chickens were maximum, the body weight of chickens with homozygote T354C was 92.12% of those with heterozygote, and the difference of the body weight between deletion homozygote and heterozygote was not significant. There was no significant difference of shank length among three genotypes.

Normal fibroblasts promote myodifferentiation of myoblasts from sex‐linked dwarf chicken via up‐regulation of β1 integrin

Fusion of monomyoblasts to form multinucleated myotubes is a prerequisite for skeletal myogenesis, and muscle fibroblast-myoblast interaction plays an important role in the process; however, relative studies are limited. In the current study, SLD (sex-linked dwarf) chicken, a myogenic deficient model caused by GH (growth hormone)-IGF-I axis deficiency due to dw gene mutation, was introduced to study effects of fibroblasts on myodifferentiation. Using a membrane insert co-culture system, we identified that, compared with SLD fibroblasts, normal fibroblasts promoted myogenesis of primary SLD myoblasts by improving their differentiation potential in a paracrine fashion, and this effect was involved in both primary and secondary fusions. This process was also coupled with up-regulation of β1 integrin, and reduced myogenesis, resulting from siRNA interference demonstrated that β1 integrin was required for the response. Further, in terms of genetic discrepancy between normal and SLD fibroblasts, GH-IGF-I signalling might play a role in this paracrine control.

Effects of the Chicken Sex-linked Dwarf Gene on rowth and Muscle Development

The aim of this study was to analyze the effects on growth and muscle development during the growing period of the sex-linked dwarf gene in the background of a Taiwan Country chicken strain, L2, selected for egg production. Eight crossbred males, heterozygous for the DW*DW mutation, were each backcrossed to six females of the L2 strain to produce two genotypes of BC females, either normal (DW*N + /-) or dwarf (DW*DW/-). The experiment included 251 normal and 207 dwarf pullets. The effect of the dwarf gene on body weight and shank length was highly significant from 2 weeks of age. The reduction of body weight by the dwarf gene reached 34.8% and 37.4% as compared to normal sibs at 16 and 20 weeks of age, respectively. Parameters of the growth curve were estimated: the age at inflection (TI) was higher in normal pullets (66.9 days) than in dwarf pullets (61.2 days). A significant effect of the dwarf gene on single muscle fiber cross-section area was found from 12 weeks of age onwards, whereas the dwarf gene had no effect on the total number of muscle fibers. Comparing the effect of the dwarf gene on shank length at different ages revealed an earlier effect on skeleton growth, observed from 2 weeks of age, than on muscle development, which was affected from 8 to 12 weeks of age. (Key Words : Growth Curve, Muscle Development, Sex-linked Dwarf Gene, Chicken)