Keragaman Genetik Dan Pendugaan Jumlah Gen Ketahanan Kacang Panjang (Vigna Sinensis L.) Terhadap Penyakit Kuning

Penyakit kuning pada kacang panjang berdampak pada penurunan produksi. Gejala serangan diawali dari gejala daun keriting serta mengakibatkan polong berwarna kuning. Penelitian ini bertujuan mengetahui nilai heritabilitas dan ragam genetik serta menduga jumlah gen pengendali ketahanan kacang panjang terhadap penyakit kuning. Penelitian dilaksanakan di Kabupaten Kediri pada bulan April sampai Juli 2013. Bahan penelitian adalah populasi UB 715 A (P1), Hitam Putih (P2), populasi F1 dan populasi F2. Berdasarkan hasil penelitian, populasi UB 715 A (P1 ) menunjukkan respon tahan terhadap penyakit kuning, populasi Hitam Putih (P2) menunjukkan respon rentan, dan populasi F1 dan F2 menunjukkan respon sedang. Karakter jumlah polong dan jumlah biji per tanaman memiliki keragaman yang sempit sedangkan karakter panjang polong, bobot segar polong, umur berbunga, dan umur panen memiliki keragaman yang luas. Karakter panjang polong dan jumlah biji per polong memiliki nilai heritabilitas rendah, sedangkan karakter jumlah polong, bobot segar polong, umur berbunga, dan umur panen memiliki nilai heritabilitas tinggi. Rasio sifat ketahanan terhadap penyakit kuning pada populasi F2 adalah 9 tahan : 3 sedang : 4 rentan yang berarti ketahanan terhadap penyakit kuning dikendalikan oleh dua gen dengan aksi gen epistasis resesif

CMR and gene sequencing.

<p>CMR images from a 25-year-old HCM patient with SRVH. RV outflow tract long-axis views during end-diastole (A) and end-systole (B) demonstrating remarkable thickening of the RV anterior wall and apical region with obstruction. A Holter recording of a non-sustained ventricular tachycardia attack. RV short-axis view (D) demonstrating extreme thickening of the RV free wall and regional transmural LGE of the RV anterior and free walls (red arrow). In the left panels, the red arrows indicate the double-peak at the site of the identified mutations. LA: left atrium; LV: left ventricle; LVOT: left ventricular outflow tract; PA: pulmonary artery; RV: right ventricle; RVAW: RV anterior wall.</p

The baseline clinical characteristics of HCM patients with SRVH and ApHCM patients.

<p>The baseline clinical characteristics of HCM patients with SRVH and ApHCM patients.</p

Histological findings.

<p>(A) Histological section of the RV free wall of an HCM patient with SRVH showing cardiomyocyte enlargement and disarray (hematoxylin-eosin staining, 200×) and (B) extensive interstitial fibrosis (Masson’s trichrome staining, 200×). (C) Histological section of the RV free wall of a patient with a double-chambered right ventricle demonstrating cardiomyocyte hypertrophy without disarray (D) and without interstitial fibrosis (E).</p

Clinical outcomes of HCM patients with SRVH and ApHCM patients during the follow-up period.

<p>Clinical outcomes of HCM patients with SRVH and ApHCM patients during the follow-up period.</p

A summary of the mutations affecting HCM patients with SRVH.

<p>A summary of the mutations affecting HCM patients with SRVH.</p

KEGG pathway enrichment analysis of differentially expressed genes.

<p>Pathways belonging to different classifications, including “Cellular Processes”, “Environmental Information Processing”, “Genetic Information Processing”, “Human Diseases” and “Metabolism”, were listed on the left of the plot. The number of genes enriched into each pathway was dotted on the corresponding dashed line. Filled circles show number of genes down-regulated during torpor, and hollow circles show number of genes up-regulated during torpor.</p

Transthoracic echocardiography and gene sequencing.

<p>An apical 4-chamber view of an 18-year-old patient with HCM demonstrating pronounced hypertrophy of the RV free wall during end-diastole (A) and RV cavity obliteration in the mid-ventricular region, as well as in the apical cavity (B). (C) Modified parasternal short-axis views with color Doppler flow mapping demonstrating striking hypertrophy of the RV anterior wall and narrowing of the RV outflow tract. (D) Color Doppler mapping demonstrating turbulent flow from the RV outflow tract to the PA (arrow). In the left panels, the red arrows indicate the double-peak at the site of the identified mutations. LA: left atrium; LV: left ventricle; LVOT: left ventricular outflow tract; PA: pulmonary artery; RA: right atrium; RV: right ventricle.</p

The number of differentially expressed genes obtained from DEGseq and GFOLD programs.

<p>(A) The number of down-regulated genes during torpor. (B) The number of up-regulated genes during torpor.</p

<i>R</i>. <i>ferrumequinum</i> liver transcriptome sequence saturation analysis and gene expression 5’~3’ bias analysis.

<p>(A) Sequence saturation analysis. (B) Sequencing 5’~3’ bias analysis. Dark red curve with solid circles represents active sample, and purple curve with solid triangles represents torpid sample.</p