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Endurance and resistance exercise training differentially impact endurance exercise capacity and fat accumulation in response to HFD feeding. (A) <t>Male</t> <t>C57BL/6J</t> mice (8–10 weeks) were separated into 4 groups differentiated by diet (normal chow vs . HFD) and exercise (sedentary vs . weightlifting (R EX ) or voluntary wheel running (E EX )) with endpoint measures made after 8 weeks of treatment. Body weight was measured weekly, and body composition was determined at the end of the study. (B) Weightlifting model and cage for R EX . (C) R EX began with 100% body weight load and increased by 20% daily until achieving 240% body weight load (8 days) where it remained for the entirety of the study. (D) Average daily lifts (repetitions) for R EX and (E) average daily kilometers for E EX . (F) Body weight gain over study period. Colored * indicates significant difference from NC-SED. (G) Body weight at endpoint. (H and I) Body composition measurements by EchoMRI for fat mass (% BW) and lean mass (g/mm tibia length). (J–L) Weight of epididymal fat, inguinal fat, and brown fat (mg) normalized by tibia length (mm). Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance among groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 10–16 (blue); HFD-E EX n : 8–15 (green). BW = body weight; E EX = endurance exercise; ETT = exercise tolerance test; GTT = glucose tolerance test; HFD = high-fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; ITT = insulin tolerance test; NC = normal chow; R EX = resistance exercise; SED = sedentary; VWR = voluntary weightlifting.
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(A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the <t>Ttc22</t> gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.
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(A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the <t>Ttc22</t> gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.
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(A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the <t>Ttc22</t> gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.
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(A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the <t>Ttc22</t> gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.
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(A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the <t>Ttc22</t> gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.
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Endurance and resistance exercise training differentially impact endurance exercise capacity and fat accumulation in response to HFD feeding. (A) Male C57BL/6J mice (8–10 weeks) were separated into 4 groups differentiated by diet (normal chow vs . HFD) and exercise (sedentary vs . weightlifting (R EX ) or voluntary wheel running (E EX )) with endpoint measures made after 8 weeks of treatment. Body weight was measured weekly, and body composition was determined at the end of the study. (B) Weightlifting model and cage for R EX . (C) R EX began with 100% body weight load and increased by 20% daily until achieving 240% body weight load (8 days) where it remained for the entirety of the study. (D) Average daily lifts (repetitions) for R EX and (E) average daily kilometers for E EX . (F) Body weight gain over study period. Colored * indicates significant difference from NC-SED. (G) Body weight at endpoint. (H and I) Body composition measurements by EchoMRI for fat mass (% BW) and lean mass (g/mm tibia length). (J–L) Weight of epididymal fat, inguinal fat, and brown fat (mg) normalized by tibia length (mm). Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance among groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 10–16 (blue); HFD-E EX n : 8–15 (green). BW = body weight; E EX = endurance exercise; ETT = exercise tolerance test; GTT = glucose tolerance test; HFD = high-fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; ITT = insulin tolerance test; NC = normal chow; R EX = resistance exercise; SED = sedentary; VWR = voluntary weightlifting.

Journal: Journal of Sport and Health Science

Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

doi: 10.1016/j.jshs.2025.101100

Figure Lengend Snippet: Endurance and resistance exercise training differentially impact endurance exercise capacity and fat accumulation in response to HFD feeding. (A) Male C57BL/6J mice (8–10 weeks) were separated into 4 groups differentiated by diet (normal chow vs . HFD) and exercise (sedentary vs . weightlifting (R EX ) or voluntary wheel running (E EX )) with endpoint measures made after 8 weeks of treatment. Body weight was measured weekly, and body composition was determined at the end of the study. (B) Weightlifting model and cage for R EX . (C) R EX began with 100% body weight load and increased by 20% daily until achieving 240% body weight load (8 days) where it remained for the entirety of the study. (D) Average daily lifts (repetitions) for R EX and (E) average daily kilometers for E EX . (F) Body weight gain over study period. Colored * indicates significant difference from NC-SED. (G) Body weight at endpoint. (H and I) Body composition measurements by EchoMRI for fat mass (% BW) and lean mass (g/mm tibia length). (J–L) Weight of epididymal fat, inguinal fat, and brown fat (mg) normalized by tibia length (mm). Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance among groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 10–16 (blue); HFD-E EX n : 8–15 (green). BW = body weight; E EX = endurance exercise; ETT = exercise tolerance test; GTT = glucose tolerance test; HFD = high-fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; ITT = insulin tolerance test; NC = normal chow; R EX = resistance exercise; SED = sedentary; VWR = voluntary weightlifting.

Article Snippet: Male C57BL/6J mice (8–10 weeks) were purchased from the Jackson Lab (Bar Harbor, ME, USA) and housed in the animal care facility under 12-h light and dark cycle standard conditions.

Techniques:

(A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the Ttc22 gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: (A) Locations of the deleted fragment (1610 bp), amplicons, gRNAs, and primers matched to the Ttc22 gene. The conservation status of Ttc22 in placental mammals, including rats, rabbits, and humans, is displayed below. (B) Characterization of Ttc22 genotypes, as determined by PCR and sequencing. The wild-type Ttc22 fragment is too long (2438 bp) to be amplified via regular PCR via the OuterF and OuterR primer sets. (C) IGV view of Ttc22 transcripts in RNA samples from the colons of three male mice with different Ttc22 genotypes, namely, Ttc22 wild-type ( Ttc22 +/+ ), heterozygously deleted ( Ttc22 +/- ), and homozygously deleted ( Ttc22 -/- ) strains, as determined by RNA sequencing. The exon 2&3 region, which is shared by both Ttc22 variants 1 and 2 and is knocked out by CRISPR-Cas9, is highlighted by a red rectangle.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques: Sequencing, Amplification, RNA Sequencing, CRISPR

(A) Illustration of wild-type Ttc22 and its TPR1- or TPR4-deleted (ΔTPR1 or ΔTPR4) expression vectors. (B) Western blot images of the full-length (FL)/wild-type Ttc22 protein and its ΔTPR1 or ΔTPR4 variant overexpressed in HEK293T cells. (C) The abundance of the Ttc22 protein in mouse colon tissues from three groups of mice, as determined by Western blotting. (D) Characterization of Ttc22 genotypes in mouse colon tissues, as determined by PCR via a pooled primer set, including OuterF, InnerF, and OuterR.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: (A) Illustration of wild-type Ttc22 and its TPR1- or TPR4-deleted (ΔTPR1 or ΔTPR4) expression vectors. (B) Western blot images of the full-length (FL)/wild-type Ttc22 protein and its ΔTPR1 or ΔTPR4 variant overexpressed in HEK293T cells. (C) The abundance of the Ttc22 protein in mouse colon tissues from three groups of mice, as determined by Western blotting. (D) Characterization of Ttc22 genotypes in mouse colon tissues, as determined by PCR via a pooled primer set, including OuterF, InnerF, and OuterR.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques: Expressing, Western Blot, Variant Assay

The appearance of C57BL/6N male and female C57BL/6N mice with different Ttc22 genotypes at approximately 66 and 77 weeks of age.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: The appearance of C57BL/6N male and female C57BL/6N mice with different Ttc22 genotypes at approximately 66 and 77 weeks of age.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques:

Mating pairs were monitored for litter production during the first pregnancy. Three pairs of wild-type ( Ttc22 +/+ ) mice and six pairs of homozygous knockout ( Ttc22 −/− ) mice were established. Each symbol represents a pair. The data are presented as the mean ± SD.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: Mating pairs were monitored for litter production during the first pregnancy. Three pairs of wild-type ( Ttc22 +/+ ) mice and six pairs of homozygous knockout ( Ttc22 −/− ) mice were established. Each symbol represents a pair. The data are presented as the mean ± SD.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques: Knock-Out

Incidence and latency period of spontaneous tumors* in C57BL/6N mice with different Ttc22 genotypes.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: Incidence and latency period of spontaneous tumors* in C57BL/6N mice with different Ttc22 genotypes.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques:

Enrichment scores for genes upregulated and downregulated by homozygous Ttc22 knockout in the colon of 57-week-old male mice.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: Enrichment scores for genes upregulated and downregulated by homozygous Ttc22 knockout in the colon of 57-week-old male mice.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques: Knock-Out

The ratio of total m6A to total adenosine in RNA (m6A/rA) in the colon tissues of mice with various Ttc22 genotypes, as determined by mass.

Journal: PLOS One

Article Title: No phenotypes in Ttc22 knockout mice

doi: 10.1371/journal.pone.0361340

Figure Lengend Snippet: The ratio of total m6A to total adenosine in RNA (m6A/rA) in the colon tissues of mice with various Ttc22 genotypes, as determined by mass.

Article Snippet: Genetically established Ttc22 knockout (Ttc22-KO) C57BL/6N mice (strain S-KO-06335) were purchased from Cyagen (Cyagen Bio.

Techniques: