scholarly journals Maternal effect of agronomical characters of F1 soybean derived from panderman variety and CpMMV-resistant soybean lines

2020 ◽  
Author(s):  
Arfiatul Isnaini ◽  
Siti Zubaidah ◽  
Heru Kuswantoro
2016 ◽  
Vol 15 (1) ◽  
pp. 1 ◽  
Author(s):  
Iswari S. Dewi ◽  
Ari C. Trilaksana ◽  
Tri Koesoemaningtyas ◽  
Bambang S. Purwoko

<p>New genetic variation in rice can be obtained by crossing between subspecies of rice (Indica, Japonica, and Javanica). Variability is a must in breeding materials. The objectives of this research were to evaluate morphological and agronomical characters of doubled-haploid lines derived from anther culture of F1 and to determine maternal effect from reciprocal crosses. The materials used in the experiment were 144 haploid lines derived from anther culture of F1 obtained from reciprocal crossing between Asemandi/Taipei 309 and Taipei 309/ Asemandi. Asemandi belongs to O. sativa subspecies Javanica, whilst Taipei 309 is subspecies Japonica. Evaluation on morphological and agronomical characters was based on Standard Evaluation System for Rice from IRRI. The results indicated that agronomical characters between haploid lines were varied, but individuals in lines were similar as shown by all morphological and agronomical characters. New characters were also found in leaf and stem angle, awn existence, awn length, awn color, panicle type and exertion, axis type, secondary branch of panicle, and grain type. Maternal effect could be seen only in booting stage, number of sterile tillers and percentage of fertile tillers. Based on number of fertile tillers, number of fertile spikelets, fertility, weight of 100 grains and yield/plant, A/T 12, A/T 57, A/T 200, A/T 274, A/T 282, A/T 321, A/T 333, A/T 348, A/T 399, A/T 75a, and T/A 258 were potential lines to be further selected.</p><p> </p><p><strong>Abstrak</strong></p><p>Variasi genetik yang baru pada padi dapat diperoleh dengan persilangan antar subspesies (Indica, Japonica, dan Javanica). Keragaman merupakan keharusan dalam materi pemuliaan. Tujuan penelitian ini ialah mengevaluasi karakter morfologi dan agronomi generasi awal galur-galur padi haploid ganda yang dihasilkan melalui kultur antera dan memeriksa pengaruh maternal yang mungkin terjadi dari persilangan resiprok. Materi yang digunakan dalam penelitian ini ialah 144 galur haploid ganda yang dihasilkan melalui kultur antera F1 dari persilangan resiprok antara Asemandi/Taipei 309 dan Taipei 309/Asemandi. Asemandi merupakan padi subspesies Javanica, sedangkan Taipei 309 merupakan subspesies Japonica. Evaluasi terhadap karakter morfologi dan agronomi dilakukan berdasarkan Standard Evaluation System for Rice dari IRRI. Hasil penelitian menunjukkan bahwa karakter antargalur haploid ganda bervariasi. Namun secara individu di dalam galur tetap serupa, sebagaimana ditunjukkan oleh semua karakter yang diamati. Karakter morfologi yang baru ditemukan pada sudut daun dan batang, keberadaan bulu, panjang bulu, warna bulu, tipe dan eksersi panikel, tipe aksis, cabang sekunder panikel, dan bentuk biji. Pengaruh maternal hanya tampak pada umur bunting, jumlah anakan tidak produktif, dan persentase anakan produktif. Berdasarkan jumlah anakan produktif, jumlah gabah isi/malai, fertilitas, bobot 100 butir, dan hasil/tanaman, maka galur dengan kode A/T 12, A/T 57, A/T 200, A/T 274, A/T 282, A/T 321, A/T 333, A/T 348, A/T 399, A/T 75a, dan T/A 258 sangat potensial untuk diseleksi lebih lanjut.</p>


Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf

Abstract We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.


Genetics ◽  
1997 ◽  
Vol 145 (1) ◽  
pp. 173-183 ◽  
Author(s):  
R Schmidt ◽  
M Hediger ◽  
R Nöthiger ◽  
A Dübendorfer

In Musca domestica, the primary signal for sex determination is the dominant factor M, which is assumed to regulate a postulated female-determining gene F. Presence of M prevents expression of F so that male development ensues. In the absence of M, F can become active, which dictates the female pathway. The existence of F is inferred from FD, a dominant factor that is epistatic to M. We describe a new mutation masculinizer, which has all the properties expected for a null or strongly hypomorphic allele of F: (1) it maps to the same chromosomal location as FD, (2) homozygous man/man animals develop as males, (3) homozygous man/man clones generated in man/+ female larvae differentiate male structures, (4) man has a sex-determining maternal effect. About a third of the morphological males synthesize yolk proteins, which indicates that they are intersexual in internal structures. The maternal effect of man is complete in offspring that derive from homozygous man/man pole cells transplanted into female hosts. In this case, all man/+ progeny become fertile males that do not produce yolk proteins. A sex-determining maternal effect has previously been demonstrated for FD. Like F, maternal man  + is needed for zygotic man  + to become active, providing further evidence that man is a loss-of-function allele of F.


Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.


Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 544
Author(s):  
Tien-Chi Huang ◽  
Kung-Chao Chang ◽  
Jen-Yun Chang ◽  
Yi-Shan Tsai ◽  
Yao-Jong Yang ◽  
...  

Placental mesenchymal dysplasia (PMD) and partial hydatidiform mole (PHM) placentas share similar characteristics, such as placental overgrowth and grape-like placental tissues. Distinguishing PMD from PHM is critical because the former can result in normal birth, while the latter diagnosis will lead to artificial abortion. Aneuploidy and altered dosage of imprinted gene expression are implicated in the pathogenesis of PHM and also some of the PMD cases. Diandric triploidy is the main cause of PHM, whereas mosaic diploid androgenetic cells in the placental tissue have been associated with the formation of PMD. Here, we report a very special PMD case also presenting with trophoblast hyperplasia phenotype, which is a hallmark of PHM. This PMD placenta has a normal biparental diploid karyotype and is functionally sufficient to support normal fetal growth. We took advantage of this unique case to further dissected the potential common etiology between these two diseases. We show that the differentially methylated region (DMR) at NESP55, a secondary DMR residing in the GNAS locus, is significantly hypermethylated in the PMD placenta. Furthermore, we found heterozygous mutations in NLRP2 and homozygous variants in NLRP7 in the mother’s genome. NLRP2 and NLRP7 are known maternal effect genes, and their mutation in pregnant females affects fetal development. The variants/mutations in both genes have been associated with imprinting defects in mole formation and potentially contributed to the mild abnormal imprinting observed in this case. Finally, we identified heterozygous mutations in the X-linked ATRX gene, a known maternal–zygotic imprinting regulator in the patient. Overall, our study demonstrates that PMD and PHM may share overlapping etiologies with the defective/relaxed dosage control of imprinted genes, representing two extreme ends of a spectrum.


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