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Even so, for multi-environment analyses, the percentage of phenotypic variance attributable to genetic effects was as expected for a complex trait, which is governed by several small effect QTLs/genes located in different genomic regions, and where the environment interactions play an important role.
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The eastern coast is marked by several small bays.
The plateau is cut by several smaller mountain ranges.
In breeding, quantitative resistance is more difficult to implement as it is mostly controlled by several genes with small effects, and it demands more effort to introgress quantitative resistance.
This may indicate that the PTA milk is a phenotype that is influenced by several markers with small effects on it, besides the possibility of epistasis and dominance, however, such genetic effects cannot be proven by the method suggested in this work.
However, more complex physiological processes relevant in the context of parallel freshwater adaptation of threespine sticklebacks are influenced by several genes, each of small effect [ 7- 10].
The poorly defined phenotypic boundaries, genetic investigations have been hampered by small effect of the identified genetic risk loci, poorly understood pathophysiology, possible contribution of several genes, and complex interactions among the genes and with the contributing environmental factors.
It is still unknown whether variation in treatment response is determined by several genes that each have a small effect size or by small numbers of genes with large effect sizes.
Our earlier QTL studies in the C×H population have shown that TYM is influenced by a major QTL with large effects, whereas SGNO is influenced by several QTL with smaller effects (R. Dolferus, X. Ji, S. Thavamanikumar, E. Tanaka, J. Edlington, K. Forrest, G. Rebetzke, M. Hayden and B. Cullis, unpublished data).
These results suggest that the detected association between stMLH and probability of breeding is driven by several loci with smaller effects and that our microsatellite-based measure of heterozygosity reflects heterozygosity over a substantial part of the genome.
The success of this approach relies on the common disease-common variant (CDCV) hypothesis, which presumes that phenotypic variation of common diseases is explained by several common variants, each with a relatively small effect [1], [2], [3].
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