ArticleGenetica2015
Genetics, realized heritability and preliminary mechanism of spinosad resistance in Phenacoccus solenopsis Tinsley (Homoptera: Pseudococcidae): an invasive pest from Pakistan.
Article in Genetica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 17 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cotton mealybug, Phenacoccus solenopsis Tinsley (Homoptera: Pseudococcidae) has gained recognition as a key pest due to its invasive nature throughout the world. The P. solenopsis has a wide range of host plants and damages the cotton crop in various parts of the world. In view of the economic importance of this pest, a study on selection, inheritance and mechanism of spinosad resistance was conducted on P. solenopsis. Selection of field collected P. solenopsis for seven generations with spinosad resulted in a high resistance ratio of 282.45-fold. Genetic studies of spinosad resistance in P. solenopsis indicated that maternal effects are not involved in spinosad resistance; and resistance development is an autosomal and incompletely dominant trait. The number of genes involved in spinosad resistance was determined to be more than one, suggesting that resistance is controlled by multiple loci. The realized heritability (h (2)) value for spinosad resistance was 0.94. Synergism bioassays of spinosad with piperonyl butoxide and S,S,S-tributyl phosphorotrithioate showed that spinosad resistance in P. solenopsis could be due to esterase only. The study provides the basic information for implementation of effective resistance management strategies to control P. solenopsis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.