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PubMed2007

Phytoplasmas: genetics, diagnosis and relationships with the plant and insect host.

Phytoplasmas cannot be cultivated in vitro, and remain the most poorly understood plant pathogens. Despite this limitation, the investigation of their nature with the aid of modern tools has produced noteworthy results during the last 20 years. Using biochemical and molecular approaches, the phylogeny of the phytoplasmas has been described, their chromosomal and extrachromosomal components are being studied, and information on the localization, movement, and metabolic interference occurring in their insect and plant hosts accumulated. At the same time, the application of the new findings in phylogeny and genetics has aided the development of powerful diagnostic tools that have improved the ability to manage diseases which are induced by phytoplasmas.

Animals↗
PubMed2006

DNA underreplication in intercalary heterochromatin regions in polytene chromosomes of Drosophila melanogaster correlates with the formation of partial chromosomal aberrations and ectopic pairing.

We studied the influence of the Suppressor of Underreplication (SuUR) gene expression on the intercalary heterochromatin (IH) regions of Drosophila melanogaster polytene chromosomes. We observed a strong positive correlation between increased SuUR expression, underreplication extent, amount of DNA truncation, and formation of ectopic contacts in IH regions. SuUR overexpression from heat shock-driven transgene results in the formation of partial chromosomal aberrations whose breakpoints map exclusively to the regions of intercalary and pericentric heterochromatin. It is important to note that all these effects are seen only if SuUR overexpression is induced during early stages of chromosome polytenization. Therefore, we developed the idea that ectopic pairing results from the joining of free DNA ends, which are formed as a consequence of underreplication.

Animals↗
PubMed2001

Peptidoglycan recognition proteins: a novel family of four human innate immunity pattern recognition molecules.

The innate immune system recognizes microorganisms through a series of pattern recognition receptors that are highly conserved in evolution. Insects have a family of 12 peptidoglycan recognition proteins (PGRPs) that recognize peptidoglycan, a ubiquitous component of bacterial cell walls. We report cloning of three novel human PGRPs (PGRP-L, PGRP-Ialpha, and PGRP-Ibeta) that together with the previously cloned PGRP-S, define a new family of human pattern recognition molecules. PGRP-L, PGRP-Ialpha, and PGRP-Ibeta have 576, 341, and 373 amino acids coded by five, seven, and eight exons on chromosomes 19 and 1, and they all have two predicted transmembrane domains. All mammalian and insect PGRPs have at least three highly conserved C-terminal PGRP domains located either in the extracellular or in the cytoplasmic (or in both) portions of the molecules. PGRP-L is expressed in liver, PGRP-Ialpha and PGRP-Ibeta in esophagus (and to a lesser extent in tonsils and thymus), and PGRP-S in bone marrow (and to a lesser extent in neutrophils and fetal liver). All four human PGRPs bind peptidoglycan and Gram-positive bacteria. Thus, these PGRPs may play a role in recognition of bacteria in these organs.

Amino Acid Sequence↗
PubMed1997

Germ-line effects of a mutator, mu2, in Drosophila melanogaster.

A mutator, mu2a, in Drosophila melanogaster potentiates terminal deficiencies. In the female germ line the gamma mutant frequency induced by irradiation of mature oocytes with 5 Gy increases approximately twofold in heterozygotes and 20-fold in homozygotes compared with wild type. The recovery of terminal deficiencies is not limited to breaks close to chromosome ends; high frequencies of deficiencies can be recovered with breakpoints located in centric heterochromatin or near the middle of a chromosome arm. Lesions induced by gamma-rays are repaired slowly in mu2a oocytes, but become "fixed" as terminal deficiencies upon fertilization. A few lesions induced in wild-type females also produce terminal deficiencies. Mutator males do not exhibit an increase in terminal deletions, regardless of the germ cell stage irradiated. In addition, there is no increase in the mutant frequency when mature sperm are irradiated and fertilize eggs produced by mu2a females. The data are consistent with the hypothesis that lesions induced in sperm chromosomes are repaired after fertilization, while lesions induced in oocyte chromosomes are shunted instead to a mechanism that stabilizes broken chromosome ends. We propose that mu2 affects chromosomal structure during oogenesis, thereby modulating DNA repair.

Animals↗
PubMed2000

Genetic screens for factors involved in the notum bristle loss of interspecific hybrids between Drosophila melanogaster and D. simulans.

Interspecific cross is a powerful means to uncover hidden within- and between-species variation in populations. One example is a bristle loss phenotype of hybrids between Drosophila melanogaster and D. simulans, although both the pure species have exactly the same pattern of bristle formation on the notum. There exists a large amount of genetic variability in the simulans populations with respect to the number of missing bristles in hybrids, and the variation is largely attributable to simulans X chromosomes. Using nine molecular markers, I screened the simulans X chromosome for genetic factors that were responsible for the differences between a pair of simulans lines with high (H) and low (L) missing bristle numbers. Together with duplication-rescue experiments, a single major quantitative locus was mapped to a 13F-14F region. Importantly, this region accounted for most of the differences between H and L lines in three other independent pairs, suggesting segregation of H and L alleles at the single locus in different populations. Moreover, a deficiency screening uncovered several regions with factors that potentially cause the hybrid bristle loss due to epistatic interactions with the other factors.

Animals↗
PubMed1993

Sex determination in Drosophila: sis-b, a major numerator element of the X:A ratio in the soma, does not contribute to the X:A ratio in the germ line.

In soma and germ cells of Drosophila, the X:A ratio builds a primary signal for sex determination, and in both tissues Sex-lethal (Sxl) function is required for cells to enter the female pathway. In somatic cells of XX animals, the products of X-chromosomal elements of the X:A ratio activate Sxl. Here I show that sisterless-b (sis-b), which is the X-chromosomal element of the somatic X:A ratio that has best been analysed, is not required for oogenesis. I also present evidence that Sxl function might not be sufficient to direct germ cells into the female pathway. These results show that the elements forming the X:A ratio in the germ line are different from the elements forming the X:A ratio in the soma and they suggest that, in the germ line, Sxl might not be regulated by the X:A ratio.

Animals↗
PubMed2026

A chromosome-scale assembly for the genome of southern corn rootworm, Diabrotica undecimpunctata.

Diabrotica undecimpunctata ssp. howardi, the southern corn rootworm or eastern 12-spotted cucumber beetle, is a generalist insect herbivore that causes damage and yield loss to several crops in North America including maize. Unresolved phylogenetic relationships within and among D. undecimpunctata subspecies are impacting current quarantine policies. We report the chromosome-level haploid genome assembly, icDiaUnde3, constructed using HiFi and Hi-C read data from a single male D. undecimpunctata collected and identified as subspecies howardi based on geographic location and morphology. The primary 1.74 Gbp assembly is scaffolded into 11 chromosome-length scaffolds representing 9 autosomes, a single X chromosome and a supernumerary (B) chromosome (scaffold N50 = 162.8 Mb and L50 = 5). Ab initio and evidence-based structural reference sequence (RefSeq) annotations predicted 18,959 protein-coding genes, in which 99.2% of the 1,367 Benchmark Universal Single-Copy Orthologs from Insecta were complete. Repeat elements occupy 1.26 Gbp (72.33%) of the icDiaUnde3 assembly, with nearly 36% predicted to be retroelements. Alignment of whole chromosomes from icDiaUnde3 with those previously assembled from Diabrotica spp. predicted 2 and 6 autosomal inversions with D. balteata and D. virgifera virgifera, respectively. The mitochondrial genome had an annotated gene order and orientation conserved among beetles. The icDiaUnde3 reference genome assembly is a vital resource for taxonomic, comparative, and functional studies to enhance sustainable crop production.

agriculture↗
PubMed1999

What is the impact of transposable elements on host genome variability?

The spread of a transposable element family through a wild population may be of astonishing rapidity. At least three families of transposable genetic elements have recently invaded Drosophila melanogaster worldwide, including the P element. The mechanism has been a process of effectively replicative transposition, and, for the P element, has occurred notwithstanding the sterility induced by unrestricted movement. This element's invasion into D. melanogaster has been accompanied by the development of heterogeneity between P sequences, most of which now have internal deletions. Increasing evidence suggests that some deleted elements can repress P transposition, thereby protecting the host from the harmful effects of complete elements. Such repressing elements may rise to high frequencies in populations as a result of selection at the level of the host. We here investigate selective sweeps invoked by the spread of P sequences in D. melanogaster populations. Numerous high-frequency sites have been identified on the X chromosome, which differ in frequency between populations, and which are associated with repression of P-element transposition. Unexpectedly, sequences adjacent to high-frequency P-element sites do not show reduced levels of genetic diversity, and DNA variability is in linkage equilibrium with the presence or absence of a P element at the adjacent selected site. This might be explained by multiple insertions or through a selection for recombination analogous to that seen in 'hitchhiking'.

Alleles↗
PubMed2000

Anopheles stephensi Dox-A2 shares common ancestry with genes from distant groups of eukaryotes encoding a 26S proteasome subunit and is in a conserved gene cluster.

The sequence of a cloned Anopheles stephensi gene showed 72% inferred amino acid identity with Drosophila melanogaster Dox-A2 and 93% with its putative ortholog in Anopheles gambiae. Dox-A2 is the reported but herein disputed structural locus for diphenol oxidase A2. Database searches identified Dox-A2 related gene sequences from 15 non-insect species from diverse groups. Phylogenetic trees based on alignments of inferred protein sequences, DNA, and protein motif searches and protein secondary structure predictions produced results consistent with expectations for genes that are orthologous. The only inconsistency was that the C-terminus appears to be more primitive in the yeasts than in plants. In mammals, plants, and yeast these genes have been shown to code for a non-ATPase subunit of the PA700 (19S) regulatory complex of 26S proteasome. The analyses indicated that the insect genes contain no divergent structural features, which taken within an appraisal of all available data, makes the reported alternative function highly improbable. A plausible additional role, in which the 26S proteasome is implicated in regulation of phenol oxidase, would also apply to at least the mammalian genes. No function has yet been reported for the other included sequences. These were from genome projects and included Caenorhabiditus elegans, Arabidopsis thaliana, Fugu rubripes, and Toxoplasma gondii. A consensus of the results predicts a protein containing exceptionally long stretches of helix with a hydrophilic C-terminus. Phosphorylation site motifs were identified at two conserved positions. Possible SRY and GATA-1 binding motifs were found at conserved positions upstream of the mosquito genes. The location of A. stephensi Dox-A2 was determined by in situ hybridization at 34D on chromosome arm 3R. It is in a conserved gene cluster with respect to the other insects. However, the A. stephensi cluster contains a gene showing significant sequence identity to human and pigeon carnitine acetyltransferase genes, therefore showing divergence with the distal end of the D. melanogaster cluster.

Amino Acid Sequence↗
PubMed1994

Function of Drosophila ovo+ in germ-line sex determination depends on X-chromosome number.

Germ-line sex determination in Drosophila melanogaster requires an assessment of the number of X chromosomes as measured against autosomal standards (XX = female, X = male) and signaling from the soma. Both of these sex determination cues are required for female-specific Sex-lethal+ function in germ cells. The ovo+ locus encodes zinc finger protein(s) required for female-specific splicing of Sex-lethal+ pre-mRNA, making ovo+ a candidate function acting between the two principal cues and Sex-lethal+. We have made ovo reporter genes and find that they show high activity in the germ line of females and low activity in the germ line of males. XY flies transformed into somatic females do not show high levels of reporter activity, while XX flies transformed into somatic males do. This shows that high level ovo+ expression depends on the number of X chromosomes, not the somatic sexual signals. The requirement for ovo+ function is restricted to XX flies. Mutations in ovo have no effect on XY males, X0 males or XY females, but have pronounced effects on germ cell viability in XX females, XX females with sex transformed germ lines, and XX males indicating that ovo+ gene products are required for events occurring only in flies with two X chromosomes.

Animals↗
PubMed2004

Lig4 and rad54 are required for repair of DNA double-strand breaks induced by P-element excision in Drosophila.

Site-specific double-strand breaks (DSBs) were generated in the white gene located on the X chromosome of Drosophila by excision of the w(hd) P-element. To investigate the role of nonhomologous end joining (NHEJ) and homologous recombination (HR) in the repair of these breaks, the w(hd) P-element was mobilized in flies carrying mutant alleles of either lig4 or rad54. The survival of both lig4- and rad54-deficient males was reduced to 25% in comparison to the wild type, indicating that both NHEJ and HR are involved in the repair P-induced gaps in males. Survival of lig4-deficient females was not affected at all, implying that HR using the homologous chromosome as a template can partially compensate for the impaired NHEJ pathway. In rad54 mutant females survival was reduced to 70% after w(hd) excision. PCR analysis indicated that the undamaged homologous chromosome may compensate for the potential loss of the broken chromosome in rad54 mutant females after excision. Molecular analysis of the repair junctions revealed microhomology (2-8 bp)-dependent DSB repair in most products. In the absence of Lig4, the 8-bp target site duplication is used more frequently for repair. Our data indicate the presence of efficient alternative end-joining mechanisms, which partly depend on the presence of microhomology but do not require Lig4.

Alleles↗
PubMedDate not supplied

Genetic resistance to afltoxin B1 toxicity in Drosophila melanogaster: chromosome substitution analysis.

Different wild-type strains of Drosophila melanogaster display variation in the ability to resist the toxic effects of continuous development from the egg stage on media supplemented with aflatoxin B1 (AFB1, a potent insect toxigenic agent and vertebrate hepatocarcinogen). The genetic basis of differences in egg-pupa development time and egg-adult viability have been investigated by chromosome substitution analysis. Five strains were studied: A-11, a "resistant" strain showing relatively little effect from the AFB1 treatments, with increased development time, reduced viability, and smaller body size); and three strains produced by chromosomal substitution from A-11 and A-9, testing the effect of either chromosome X (strain R-X), 2 (strain R-2) or 3 (strain R-3) from A-11 against an A-9 background. Data from R-X, R-2, and R-3 indicate that autosomal genes on chromosomes 2 and 3 control the ability of strain A-11 to resist the toxic effects of AFB1 ingestion during larval development.

Aflatoxins↗
PubMed1998

A chitinase encoding gene (chit1 gene) from the entomopathogen Metarhizium anisopliae: isolation and characterization of genomic and full-length cDNA.

There are no reports to date of entire gene sequences coding for chitinolytic enzymes from entomopathogenic fungi, even though these enzymes act synergistically with proteolytic enzymes to solubilize insect cuticle during the key step of host penetration, having considerable importance in the biological control of some insect pests. This paper reports the complete nucleotide sequence and analysis of the chromosomal and full-length cDNA copies of the regulated gene (chit1) coding one of the chitinases produced by the biocontrol agent Metarhizium anisopliae. Degenerated primers, encompassing conserved regions of other fungal chitinases, were used to amplify a 650-bp DNA fragment, which was used to isolate genomic and cDNA clones from M. anisopliae. Albeit at least two different chitinases are characterized in this fungus, only one chit gene was isolated. The chit1 gene is interrupted by three short typical fungal introns and has a 1,521-bp ORF, which encodes a protein of 423 amino acids with a stretch of 35 amino acid residues displaying characteristics of signal peptide. The deduced sequence of the mature protein predicts a 42-kDa protein with pI of 5.8. Southern analysis of genomic DNA indicates a single copy of chit1 in the M. anisopliae genome.

Amino Acid Sequence↗
PubMed1995

Phosphatidylserine decarboxylase 2 of Saccharomyces cerevisiáe. Cloning and mapping of the gene, heterologous expression, and creation of the null allele.

The yeast Saccharomyces cerevisiae expresses two phosphatidylserine decarboxylase (PSD) activities which are responsible for conversion of phosphatidylserine to phosphatidylethanolamine, and either enzyme alone is sufficient for normal cellular growth. However, strains containing a PSD1 null allele and a mutation leading to loss of PSD2 activity (psd1-delta 1::TRP1 psd2) are auxotrophic for ethanolamine. This nutritional requirement was utilized to isolate the gene encoding the PSD2 enzyme by complementation. The PSD2 gene encodes a protein of 1138 amino acids with a predicted molecular mass of 130 kDa. The deduced amino acid sequence shows significant identity (34%) to a PSD-like sequence from Clostridium pasteurianum and the yeast PSD1 (19%) at the carboxyl end of the protein. Of particular interest is the presence of a sequence, GGST, which may be involved in post-translational processing and prosthetic group formation similar to other PSD enzymes. The PSD2 amino acid sequence also shows significant homology to the C2 regions of protein kinase C and synaptotagmin. Physical mapping experiments demonstrate that the PSD2 is located on chromosome 7. The PSD2 gene was heterologously expressed by infection of Sf-9 insect cells with recombinant baculovirus, resulting in a 10-fold increase in PSD activity. The null allele of PSD2 was introduced into yeast strains by one-step gene deletion/disruption with a HIS3 marker gene. Strains expressing wild type PSD1 and the psd2-delta 1::HIS3 allele show a small decrease in overall PSD activity, but no noticeable effect upon [3H]serine incorporation into aminophospholipids. Strains containing both the psd1-delta 1::TRP1 and psd2-delta 1::HIS3 null alleles, however, express no detectable PSD activity, are ethanolamine auxotrophs and show a severe deficit in the conversion of [3H]serine-labeled phosphatidylserine to phosphatidylethanolamine. These data indicate that the gene isolated is the structural gene for PSD2 and that the PSD1 and PSD2 enzymes account for all yeast PSD activity.

Alleles↗
PubMed2005

Massive genome erosion and functional adaptations provide insights into the symbiotic lifestyle of Sodalis glossinidius in the tsetse host.

Sodalis glossinidius is a maternally transmitted endosymbiont of tsetse flies (Glossina spp.), an insect of medical and veterinary significance. Analysis of the complete sequence of Sodalis' chromosome (4,171,146 bp, encoding 2,432 protein coding sequences) indicates a reduced coding capacity of 51%. Furthermore, the chromosome contains 972 pseudogenes, an inordinately high number compared with that of other bacterial species. A high proportion of these pseudogenes are homologs of known proteins that function either in defense or in the transport and metabolism of carbohydrates and inorganic ions, suggesting Sodalis' degenerative adaptations to the immunity and restricted nutritional status of the host. Sodalis possesses three chromosomal symbiosis regions (SSR): SSR-1, SSR-2, and SSR-3, with gene inventories similar to the Type-III secretion system (TTSS) ysa from Yersinia enterolitica and SPI-1 and SPI-2 from Salmonella, respectively. While core components of the needle structure have been conserved, some of the effectors and regulators typically associated with these systems in pathogenic microbes are modified or eliminated in Sodalis. Analysis of SSR-specific invA transcript abundance in Sodalis during host development indicates that the individual symbiosis regions may exhibit different temporal expression profiles. In addition, the Sodalis chromosome encodes a complete flagella structure, key components of which are expressed in immature host developmental stages. These features may be important for the transmission and establishment of symbiont infections in the intra-uterine progeny. The data suggest that Sodalis represents an evolutionary intermediate transitioning from a free-living to a mutualistic lifestyle.

Adaptation, Physiological↗
PubMed2005

Endogenous retroviruses and animal reproduction.

Endogenous retroviruses (ERV), as part of the host genetic heritage, are transmissible to the next generation in a Mendelian way. Their abundance in animal genomes and their expression primarily detected in germ cells, embryonic tissues and cancer cell lines, raised the question of their biological significance. This article reviews the possible role of ERVs in the physiology and diseases of animal reproduction, from Drosophila to human. In males, there is no trivial involvement of ERVs in a physiological process. Conversely, a spermatogenesis defect was associated in the human male with HERV-K expression and HERV15-induced chromosomal alteration, leading to cancer and infertility, respectively. In females, the study of insect ERVs (IERV) pointed out the overlap between genetics and virology with the genetic-dependent regulation of ZAM and the non-infectious and infectious life cycles of gypsy. The pattern of ERVs expression in rodent, ovine and human females suggest a hormone-dependent mechanism consistent with the mammalian oestrus cycle regulation. The differentiation of the mammary epithelium and breast tumorigenesis involving the mouse mammary tumour viruses (MMTV) illustrate the intimate connection between endogenous and exogenous retroviruses. Last, as a major site of ERVs transcription, placenta contributed to our understanding of ERVs modulation of neighbouring gene expression. As an interface, i.e. a site of conflicts and exchanges, placenta should resist infection and protect the foetus against the maternal immune system. Retroviral envelopes could theoretically provide such features due to receptor interference, immunosuppression and fusion properties, as shown by the HERV-W envelope involved in the syncytiotrophoblast formation. We conclude with an insight on the evolutionary and epigenetic consequences of the relationships of ERV guests with their animal hosts.

Animals↗
PubMed1981

Possibilities for genetic manipulation of sex ratio in livestock.

Reports are reviewed in which genetic differences for sex ratio of offspring were found among breeds, breed crosses, strains, lines, line crosses, families or individuals. Although reports in which genetic variation could not be identified outnumber those in which it could, important genetic variation does exist in at least some populations. The direct or correlated response of sex ratio to selection is reviewed. Again, results are equivocal, but there is ample evidence that sex ratio will respond to selection in at least some populations of laboratory organisms. Segregation distortion in the mouse and in Drosophila is examined. Segregation distortion occurs when a heterozygous male mated to a homozygous female does not produce the two offspring types in equal proportions and the disparity cannot be accounted for by sampling or differential mortality. Although the most well-known systems have no effect (in the mouse) or only a moderate effect (in Drosophila) on sex ratio, systems in which sex ratio is subject to segregation distortion are known to exist in insects and could exist in mammals. Finally, the possibility is discussed that XX/XY chromosome chimaeric bulls, born co-twin to a heifer, might produce a preponderance of heifer progeny. A few reports suggest this might be the case, but other research is not in agreement.

Animals↗