Chromosome abnormalities in Japanese quail embryos

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Chromosome abnormalities in Japanese quail embryos

Ca de la Sena, Ns Fechheimer, Ke Nestor

To cite this version:

Chromosome abnormalities

in

_Japanese

_{quail embryos}

CA de la Sena

NS

Fechheimer

KE Nestor

The Ohio State

_{University, Departments of ’Molecular Genetics,}

2

Dairy

Science and

₃

_Poultry

_{Science, Columbus, OH,}

USA

(Proceedings

of the 9th

_European

_Colloquium

on

_Cytogenetics

of Domestic

_Animals;

Toulouse-Auzeville,

10-13

_July

₁₉₉₀₎

Japanese quail

/

embryos

/

heteroploidy

/

chromosomes

INTRODUCTION

Embryos

of the domestic chicken have been used

_extensively

to elucidate

_questions

regarding

the extent to which

_heteroploidy

is a cause of

_{embryonic mortality,}

the

sources of errors

_leading

to various

_types

of

_heteroploid

_zygotes

and the

_etiology

of

_heteroploid

_zygotes

and

embryos

(Fechheimer,

1981,

1990).

The

_{Japanese quail}

possesses many of the attributes of the

chicken,

as well as others that contribute further to its usefulness for such work.

_Quail

hens have a mature

_{body weight}

of

_only

about 100 g,

produce

eggs at the same rate as chickens and reach sexual

_maturity

at about 6 weeks of _age. The incubation

_period

is

_only

18

_days.

The

_karyotype

of the

_quail

is similar to that of

_chicken,

_comprising

38

_pairs

of autosomes and

Z and W gonosomes.

Eight

autosomal

pairs

and the Z and W are

relatively

long

and have

_sufficiently

distinctive

_morphology

that each can be

readily recognized

in

_{metaphase plates}

_(Talluri

and

_Vegni,

_1965;

Ansari and

_Singh,

_1983).

The W is

largely

heterochromatic and stains

_densely

when

_C-banding

_procedures

are

_applied.

Variants of chromosomes 4 and Z have been identified

_by

_C-banding

in several

populations

and are valuable as markers.

The

_present

_study

was undertaken to

_explore

the

_suitability

of

_{Japanese quail}

as a model vertebrate

_system

in which

_genetic

factors

might

be identified that

disrupt

the

_orderly

sequence of the

reproductive cycle,

thus

resulting

in the occurrence of

various

_types

of

_heteroploidy

in

_embryos.

MATERIALS AND METHODS

A

_population

of

_{Japanese quail}

is maintained

_{by mating}

of 36

_pairs.

The male and

female for each

_{paired mating}

are chosen at random. The 36 males and females *

To whom

_{correspondence}

should be addressed:

_Department

of

_{Dairy Science,}

2027

_Coffey

represent each of the 36 families

_(Nestor

et

_al,

_1982).

In the

_present

_{study, matings}

were made between 36

_pairs

of full

_sibs,

one

_pair

from each of the families of the

randomly

mated

_population.

_Eggs

were collected in sufficient

_quantity

to enable

karyological

analysis

of 20

_embryos

from each

_family.

Additional eggs were then

incubated to

_reproduce

the

_family.

Infertile

_pairs

were

_{replaced by}

additional

_pairs

from the same

family

when it was

_possible

to do so.

_Otherwise,

_replacements

were

chosen from one of the other

_remaining

families. The _process was

repeated

for 3

generations.

Following

16 h of

_incubation,

_eggs were

_injected

with 0.06 ml of a

0.2%

solution of colchicine and returned to the incubator for 2 h.

_Embryos

were

_prepared

for

karyological

examination

_according

to the

_procedure

of Miller et al

₍₁₉₇₁₎

that has

been

_{applied extensively}

for chicken

_embryos.

_Routinely,

10 cells from each

_embryo

were examined. If one or more was

_aberrant,

additional cells were examined to

establish the extent of

_mixoploidy.

Analysis

of variance was

_applied,

_using

two different

models,

to test for

signi-ficance of differences in the incidences of each

_type

of

_abnormality

among the 36

inbred lines

_(lineages)

and 107 full sib families each of which

_comprised

about 20

embryos.

RESULTS AND DISCUSSION

A total of 2 893 eggs was

_inspected,

of which 2 037

(70%)

contained

_embryos

that were

successfully

_analyzed.

Of the

_remainder,

17%

were

_infertile,

4.8%

contained

dead

_embryos,

3.2%

were

_{destroyed during}

_processing

and

4.6%

contained live

embryos

that could not be

_analyzed

because too few

_{metaphase plates}

were

_present

on the slide.

The

_frequencies

of various

_types

_{of heteroploid}

_embryos,

_embryos

in which one or more cells contained a structural aberration and

_embryos

in which all the

chromo-somes in all cells exhibited a

_particular

_{atypical configuration}

are shown in table I. The overall

_frequency

of

_{embryos bearing}

chromosome abnormalities was

15.3%

and all

_categories

of

abnormalities,

except

aneuploidy

and structural

aberrations,

had

_frequencies

of

1.0%

or

_greater.

Aneuploidy

was

relatively infrequent

because

it could be observed for

_only

8 of the 38

_pairs

of

_autosomes;

4 of the

_aneuploids

involved the sex chromosomes.

For several of the

_types

of

_{heteroploidy,}

the

_origins

of the error can be inferred

from their sex chromosome

_complements

or

_{by analogy}

with similar observations

of chicken

embryos

bearing

marker chromosomes that were

_possessed

_{by only}

one

parent

(Fechheimer

and

_Jaap,

_1978,

_1980).

The

_presumed

or known sites of

_origin

for each

_type

of

_abnormality

are

_given

in table I.

_Arguments

in

_support

of these

inferences are

_given

in a

_previous

communication

_(Fechheimer,

_1981).

Of

_particular

interest is a new

_type

of aberration referred to as

_atypical

mitotic

metaphase.

This aberration is characterized

_{by metaphase}

chromosomes with the

two chromatids

_parallel

to one another and not

_exhibiting

the usual constriction at

the centromere

_region.

It is unlike other

similar,

previously

described

_aberrations,

such as

C-mitosis, endoreduplication

and

_premature

centromere division. It was seen

only

5 of the 107

families,

indicating

that the

_anomaly

is

_probably

caused

_by

a

genetic

factor.

The results of

_analysis

of variance for differences in

_frequency

of the several abnormalities among families and

lineages

is shown in table I.

_Significant

differences

are

interpreted

as non-random distribution of a

particular

abnormality

_among

families or

_lineages.

Such non-random

_{distribution, ie,}

_clustering,

is considered

to be

_strong

evidence for

_genetic

influence as an

_etiological

element.

_Triploidy,

haploidy,

diploid/tetraploid

mosaicism and

atypical

mitotic

_metaphase

all were

found to cluster within certain families and both

_triploidy

and

_haploidy

as well as

aneuploid

mosaicism were found to be

_non-randomly

distributed among

lineages.

No evidence for

_genetic

control of

_aneuploidy

or structural aberrations was found.

From 36 inbred lines started from a

_randomly

mated

_population,

_only

16

survived to

_{produce embryos}

in the third

_generation.

The

_remaining

20

_lineages

could not be continued because full sib

_matings

did not

_yield

viable and fertile

only

36

_original

_matings,

evidence was obtained for the existence of _{mutant genes,}

segregating

in the random

_{mating population,}

that

detrimentally

affect several

stages

of the

_{reproductive cycle.}

Interference with the normal course of both first

and second meiotic divisions is indicated

_by

the

_triploids.

Anomalies of fertilization resulted in the occurrence of the

_haploid

chimeras and a few of the

_triploids.

Disruption

of normal mitosis

_{during cleavage}

divisions resulted in

_production

of

diploid/tetraploid

and

_{diploid/aneuploid}

_mosaics,

and the aberration called

_atypical

mitotic

_metaphase.

It is reasonable to _suppose that genes with such detrimental effects occur at low

frequencies

in the base

_population.

Because each

_lineage

was

_reproduced

in each

generation

from

_only

two

_parents,

a

large

proportion

of such genes was eliminated

from each

_lineage,

by chance,

in 3

_generations

of full sib

_{mating. Therefore,}

the detection of the occurrence of a few genes that cause

_disruption

of meiosis and

mitosis in this

_experiment

indicates that

_probably

_many more were

_present

in

the base

population.

It should be

possible

to detect many of them

by

further

experimentation

with this or similar

populations

of

Japanese quail.

The

Japanese

quail

appears to

_provide

an excellent vertebrate

_system

for the detection and

subsequent

characterization of meiotic and mitotic mutant _genes similar to those that have been so

_thoroughly

studied in

_yeast,

_drosophila

and

_plants

(reviewed

_by

Baker et

_al,

_1976).

ACKNOWLEDGMENTS

Gratitude is extended to Mr John Anderson who

provided

excellent care for the

experi-mental animals. Salaries and research support were

_partly

provided by

funds

appropriated

to The Ohio

_Agricultural

Research and

_Development

Center.

REFERENCES

Ansari

_{HA, Singh}

H

₍₁₉₈₃₎

The chromosome

_complements

of

Japanese quail

(Coturnix

coturnix

_japonica).

Avian Res

_67,

81-84

Baker

BS, Carpentier ATC, Esposito MS, Esposito RE,

Sandler L

₍₁₉₇₆₎

Genetic control of meiosis. Annu Rev Genet

_10,

53-134

Fechheimer NS

_{(1981) Origins}

of

_heteroploidy

in chick

embryos.

Poult Sci 60, 1365-1371

Fechheimer NS

₍₁₉₉₀₎

The domestic chicken

_{(Gallus domesticus)}

as an

_organism

for the

study

of chromosomal aberrations. In: Farm Animals in Biochemical Research

_(Pliska

_V,

Stranzinger G,

eds).

Verlag

Paul

_{Parey, Hamburg}

Fechheimer

_{NS, Jaap}

RG

₍₁₉₇₈₎

The

_parental

sources of

heteroploidy

in chick

embryos

determined with

_{chromosomally}

marked gametes. J

Reprod

Fertil

52,

141-146

Fechheimer

_NS,

_Jaap RG

_{(1980) Origins}

of

_euploid

chimerism in

_embryos

of Gallus

do7nesticus. Genetica

_52/53,

69-72

Miller

_RG,

Fechheimer

_{NS, Jaap}

RG

₍₁₉₇₁₎

Chromosome abnormalities in 16- to 18-hour chick

_{embryos. Cytogenetics}

10, 121-136

Nestor KE, Bacon

_WL,

Lambio AL

₍₁₉₈₂₎

_Divergent

selection for

_{body weight}

and

_yolk

precursor in Coturnix coturnix japonica. 1. Selection response. Poult Sci 61, 12-17 Talluri

_{MV, Vegni}

L

₍₁₉₆₅₎

Fine resolution of the

_karyogram

of the

_quail

Coturnix coturnix