Hereditas (Hereditas)

Publisher: Mendelian Society of Lund, Mendelian Society of Lund

Journal description

Hereditas is a well established journal in the field of genetics and cytogenetics. It was founded in 1920, and publishes original research and reviews from all sections of genetics.

Current impact factor: 1.12

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 1.118
2013 Impact Factor 0.756
2012 Impact Factor 0.964
2011 Impact Factor 0.788
2010 Impact Factor 1.066
2009 Impact Factor 0.873
2008 Impact Factor 1.175
2007 Impact Factor 0.84
2006 Impact Factor 1.269
2005 Impact Factor 0.596
2004 Impact Factor 0.69
2003 Impact Factor 0.564
2002 Impact Factor 0.53
2001 Impact Factor 0.711
2000 Impact Factor 0.753
1999 Impact Factor 0.855
1998 Impact Factor 0.907
1997 Impact Factor 0.4
1996 Impact Factor 0.545
1995 Impact Factor 0.647
1994 Impact Factor 0.774
1993 Impact Factor 0.669
1992 Impact Factor 0.616

Impact factor over time

Impact factor

Additional details

5-year impact 0.91
Cited half-life >10.0
Immediacy index 0.11
Eigenfactor 0.00
Article influence 0.26
Website Hereditas website
Other titles Hereditas (Online)
ISSN 1601-5223
OCLC 51050025
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Mendelian Society of Lund

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Publisher's version/PDF may be used
    • Authors retain copyright
    • All titles are open access journals
  • Classification

Publications in this journal

  • No preview · Article · Dec 2015 · Hereditas

  • No preview · Article · Jan 2015 · Hereditas
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    ABSTRACT: In 1928, the Swedish geneticists Hermann Nilsson-Ehle and Åke Gustafsson started on their suggestion experiments with induced mutations using the barley crop. In 1953, at the instigation of the Swedish Government, the 'Group for Theoretical and Applied Mutation Research' was established. Its aim was to study basic research problems in order to influence and improve methods for breeding cultivated plants. The research was non-commercial, even if some mutants were of practical importance. The peaks of activities occurred during the 1950s, 1960s and 1970s. Applying X-rays and UV-irradiation very soon the first chlorophyll mutations were obtained followed by the first viable mutations 'Erectoides'. Soon the X-ray experiments expanded with other types of irradiation such as neutrons etc. and finally with chemical mutagens, starting with mustard gas and concluding with the sodium azide. The research brought a wealth of observations of general biological importance, high increased mutation frequencies, difference in the mutation spectrum and to direct mutagenesis for specific genes. A rather large collection of morphological and physiological mutations, about 12 000 different mutant alleles, with a very broad variation were collected and incorporated into the Nordic Genetic Resource Center (NordGen) Sweden. Barley, the main experimental crop has become one of the few higher plants in which biochemical genetics and molecular biological studies are now feasible. The collection is an outstanding material for mapping genes and investigating the barley genome. Several characters have been studied and analyzed in more detail and are presented in this historical review. © 2014 The Author.
    Preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: The Mendelian Society in Lund was founded in 1910. The initiative came from two young biologists supported by a wide circle of interested plant breeders and academics. Already from the start the society was dominated by the towering personality Herman Nilsson-Ehle. After two active years, the Society went into temporal hibernation until it resumed its activities in spring 1916, when Nilsson-Ehle was on his way to become Sweden's first professor of genetics. One of the aims of the Society was to launch a scientific journal for local scientists directed at an international audience. After a successful fundraising campaign, Hereditas was started in 1920. One of the original instigators of the Mendelian Society, Robert Larsson, became its first editor, and he remained in this position for more than 30 years. Both he and Nilsson-Ehle were fascinating personalities, deeply rooted in their time's scientific and ideological debates. © 2014 The Authors.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: Gunnar Ostergren (1918-1998), a cytologist-geneticist of rank (Fig. 1), was active at the Inst. of Genetics, Univ. of Lund (Sweden) during the years 1940-1964, intermitted by a stay in Stockholm (Nobel Institute, 1947-1951), and followed by being a professor of genetics, and later professor emeritus, at the Swedish Univ. of Agricultural Sciences in Uppsala (1964-1998). Gunnar Ostergren (G.O.) had connections with HEREDITAS in two ways. Firstly, during the years at the Inst. of Genetics in Lund, where the editorial office of HEREDITAS was located, he assisted in the editorial work of this periodical by handling the pictorial material of accepted articles. This task was handed over to me when he left for Uppsala, after giving me useful guidelines that I made use of during my years at this post. Secondly, HEREDITAS was the forum where he published the majority of his work. His most cited publication is his PhD thesis on chromosome orientation during cell division (Ostergren 1951), briefly highlighted here. This work laid the grounds for, and was ratified by, recent findings. In addition to these connections to HEREDITAS that motivated me to write about G.O. is the fact that he has been my supervisor and mentor during the time I worked for my PhD degree (1958-1963). My respect and admiration of G.O. is great.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: Two papers published in HEREDITAS between 1921 and 1939 show how the attitude towards race biology changed in the course of the interwar period in the Nordic countries. In the early 1920s race biology was seen to constitute a legitimate science. Ordinary human genetics prevailed, however, over race biology already in the very beginning on the pages of HEREDITAS. Population thinking was introduced into the study of human heredity around the year 1930. It effectively contradicted the concept of the race. Interestingly, HEREDITAS does not carry a single paper on eugenics and sterilization. In 1939 we see a final repudiation of the doctrines on race. Times had changed and the National Socialists had usurped the doctrines of race in Germany. © 2015 The Author.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: Notch signalling mediates intercellular communication, which is effected by the transcription factor CSL, an acronym for vertebrate CBF1/RBP-J, Drosophila Suppressor of Hairless [Su(H)] and C. elegans Lag1. Nuclear import of CBF1/RBP-J depends on co-activators and co-repressors, whereas the export relies on RITA. RITA is a tubulin and CBF1/RBP-J binding protein acting as a negative regulator of Notch signalling in vertebrates. RITA protein is highly conserved in eumatazoa, but no Drosophila homologue was yet identified. In this work, the activity of human RITA in the fly was addressed. To this end, we generated transgenic flies that allow a tissue specific induction of human RITA, which was demonstrated by Western blotting and in fly tissues. Unexpectedly, overexpression of RITA during fly development had little phenotypic consequences, even when overexpressed simultaneously with either Su(H) or the Notch antagonist Hairless. We demonstrate the in vivo binding of human RITA to Su(H) and to tubulin by co-immune precipitation. Moreover, RITA and tubulin co-localized to some degree in several Drosophila tissues. Overall our data show that human RITA, albeit binding to Drosophila Su(H) and tubulin, cannot influence the Notch signalling pathway in the fly, suggesting that a nuclear export mechanism of Su(H), if existent in Drosophila, does not depend on RITA. © 2015 The Authors.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: GRM8 is a schizophrenia candidate gene that is also thought to be involved in the glutamate pathway, which is very important in the pathogenesis of schizophrenia. In this study, we aim to investigate the association between GRM8 and schizophrenia in the Uygur Chinese population. Rs2237748 and rs2299472, located in the GRM8 gene, were selected for genotyping in a set of Uygur Chinese case-control samples, which included 723 cases and 561 controls, using TaqMan assays and capillary sequencing. The statistical analysis was carried out using the online software program SHEsis, and a meta-analysis was carried out to identify other relevant studies using Review Manager 5. We found that the rs2299472 genotype was significantly associated with schizophrenia (P = 0.015, P = 0.030, after Bonferroni correction). The frequency of the CC genotype was higher in the schizophrenic patients (P = 0.008), and the frequency of the AC genotype was lower (P = 0.008). Furthermore, the meta-analysis incorporating the previous and current studies also showed that rs2299472 is associated with schizophrenia. This study indicates that the GRM8 gene may play an important role in the pathogenesis of schizophrenia. © 2015 The Authors.
    Preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: In this study part of the mitochondrial D-loop was sequenced in a total of 40 samples from nine Swedish local chicken breeds. Among our 40 samples we observed 15 segregating sites and seven different haplotypes. The most common haplotype was present in all investigated individuals in five breeds and together with other haplotypes in three breeds. This haplotype is common in domestic chickens and has been found in both local and commercial breeds in many parts of the world. The breed Ölandshöna was most different from the other Swedish breeds with all three individuals sharing a haplotype that differed from the most common haplotype at nine of the 15 segregating sites.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: In 1921 Hereditas published an article on the fall of Rome written by the famous classical scholar Martin P:son Nilsson. Why was a paper on this unexpected topic printed in the newly founded journal? To Nilsson, the demise of the Roman Empire was explained by the "bastardization" occurring between "races" from different parts of the realm. Offspring from mixed couples were of a less stable "type" than their parents, due to the breaking up by recombination of the original hereditary dispositions, which led to a general loss of competence to rule and govern. Thus, the "hardness" of human genes, together with their recombination, was - according to Nilsson - the main cause of the fall of Rome. Nilsson's argument is not particularly convincingly presented. Human "races" are taken to have the same genetic structure as inbred crop strains, and Nilsson believes in a metaphysical unity between the individual and the race to which it belongs. However, in my view, Martin P:son Nilsson and his friend Herman Nilsson-Ehle had wider aims with the article than to explain a historical event. The article can be read as indicating strong support from the classical human sciences to the ambitious new science of genetics. Support is also transferred from genetics to the conservative worldview, where the immutability and inflexibility of the Mendelian genes are used to strengthen the wish for greater stability in politics and life. The strange article in Hereditas can, thus, be read as an early instance in the - still ongoing - tug-of-war between the conservative and the liberal ideological poles over how genetic results best are socially interpreted. © 2015 The Authors.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: MicroRNAs (miRNAs) are approximately 21 nt noncoding RNAs that influence the phenotypes of different species through the post-transcriptional regulation of gene expression. Although many miRNAs have been identified in a few model plants, less is known about miRNAs specific to cucumber (Cucumis sativus L.). In this study, two libraries of cucumber RNA, one based on fruit samples and another based on mixed samples from leaves, stems, and roots, were prepared for deep-sequencing. A total of 110 sequences were matched to known miRNAs in 47 families, while 56 sequences in 46 families are newly identified in cucumber. Of these, 77 known and 44 new miRNAs were differentially expressed, with a fold-change of at least 2 and p-value < 0.05. In addition, we predicted the potential targets of known and new miRNAs. The identification and characterization of known and new miRNAs will enable us to better understand the role of these miRNAs in the formation of cucumber fruit.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: The Enhancer of split complex [E(spl)-C] comprises twelve genes of different classes. Seven genes encode proteins of with a basic-helix-loop-helix-orange (bHLH-O) domain that function as transcriptional repressors and serve as effectors of the Notch signalling pathway. They have been named E(spl)m8-, m7-, m5-, m3-, mβ-, mγ- and mδ-HLH. Four genes, E(spl)m6-, m4-, m2- and mα-BFM are intermingled and encode Notch repressor proteins of the Bearded-family (BFM). The complex is split by a single gene of unrelated function, encoding a Kazal-type protease inhibitor (Kaz-m1). All members within a family, bHLH-O or BFM, are very similar in structure and in function. In an attempt to generate specific mutants, we have mobilised P-element constructs residing next to E(spl)m7-HLH and E(spl)mγ-HLH, respectively. The resulting deletions were mapped molecularly and by cytology. Two small deletions affected only E(spl)m7-HLH and E(spl)mδ. The deficient flies were viable without apparent phenotype. Larger deletions, generated also by X-ray mutagenesis, uncover most of the E(spl)-C. The phenotypes of homozygous deficient embryos were analysed to characterize the respective loss of Notch signalling activity.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: We studied and established a DNA database of 15 Y-STRs (DYS438, DYS446, DYS391, DYS390, DYS458, DYS534, DYS426, DYS626, DYS504, DYS505, DYS576, DYS532, DYS594, DYS522, DYS540) in a population sample of 102 unrelated, healthy, male individuals of Henan Han population. Allelic frequencies and statistical parameters of Han population were calculated. Totally 90 alleles were observed, with the corresponding allelic frequencies ranging from 0.0098 to 0.9020. 102 haplotypes were found in the studied group, the haplotype diversity for 15 Y-STR loci was 1. The results of present study were valuable for human identification and paternity tests routine forensic applications in the region.
    No preview · Article · Dec 2014 · Hereditas
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    ABSTRACT: Cellular differentiation during eumetazoan development is based on highly conserved signalling pathways. Two of them, the Notch and the EGFR signalling pathways, are closely intertwined. We have identified two potential target sites of the Mitogen activated kinase (MAPK), the downstream effector kinase of EGFR, within Hairless (H), the major antagonist of Notch signalling in Drosophila. Assuming that phosphorylation of these sites modulates H activity, a direct influence of EGFR signalling on Notch pathway regulation might be possible. This hypothesis was tested by generating a phospho-deficient and a phospho-mimetic H isoform and by assaying for their biological activity. We first addressed the binding of known H interaction partners Su(H), Gro, CtBP and Pros26.4 which was similar between mutant and wild type H. Next we assayed eye, wing and bristle development which are strongly affected by the overexpression of H due to the inhibition of Notch signalling. Overexpression of the mutant constructs resulted in phenotypes similar to wildtype H overexpression, yet with subtle differences in phenotypic severity. However, large variations suggest that the mutated residues may be critical for the overall structure or stability of H. Albeit of minor impact, EGFR may fine tune Notch signalling via MAPK dependent phosphorylation of H.
    No preview · Article · Oct 2014 · Hereditas