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When crossing pea plants, Mendel noticed that one of the parental traits would sometimes disappear in the first generation of offspring, called the F1 generation, and could reappear in the next generation (F2). He concluded that one of the traits must be dominant over the other, thereby causing masking of one trait in the F1 generation. When he crossed the F1 plants, he found that 75% of the offspring in the F2 generation had the dominant phenotype, while 25% had the recessive phenotype.

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Related Experiment Video

Updated: Jun 30, 2026

Isolation of High-density Lipoproteins for Non-coding Small RNA Quantification

Isolation of High-density Lipoproteins for Non-coding Small RNA Quantification

Published on: November 28, 2016

Inheritance of LDL peak particle diameter: results from a segregation analysis in Israeli families.

Y Friedlander¹, J D Kark, R Sinnreich

¹Department of Social Medicine, Hebrew University-Hadassah School of Public Health, Jerusalem, Israel. yfried@vms.huji.ac.il

Genetic Epidemiology

|April 20, 1999

Summary

This summary is machine-generated.

Genetic factors significantly influence LDL peak particle diameter (LDL-PPD), suggesting a major gene plays a key role. This finding enhances understanding of LDL particle size genetics.

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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation

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Published on: January 28, 2021

Area of Science:

Genetics
Cardiovascular Health
Biochemistry

Background:

Low-density lipoprotein particle size is a key determinant of cardiovascular disease risk.
Understanding the genetic and environmental influences on LDL peak particle diameter (LDL-PPD) is crucial for personalized medicine.

Purpose of the Study:

To investigate the genetic and environmental determinants of LDL peak particle diameter (LDL-PPD).
To identify the underlying genetic models that best explain the variation in LDL-PPD.

Main Methods:

Analysis of LDL-PPD in 80 kindreds (373 individuals) in Israel.
Sex and age adjustment of LDL-PPD data.
Application of commingling and complex segregation analyses, including a regression model with ousiotype-specific coefficients.

Main Results:

Commingling analysis indicated a mixture of two normal distributions for adjusted LDL-PPD.
A major Mendelian model was not rejected, while a mixed environmental model was rejected.
Genotypes determined by a major gene, associated with different phenotypic variances, are likely determinants of LDL-PPD.

Conclusions:

A major gene significantly influences LDL peak particle diameter.
This genetic influence, rather than environmental factors, is the primary driver of LDL-PPD variation.
The findings contribute to a better understanding of the genetics of LDL particle size.