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MINGGU XII

PLASTIDA
MITOKONDRIA
PLASTIDA
Organel sel Tumbuhan
Asal : proplastida dlm sel
meristem
Perubahan proplastida
sesuai kebutuhan sel
(lokasi pertumbuhan &
kondisi cahaya)

Perkembangan plastida:
- Etioplas / Leukoplas
- Amiloplas
- Kromoplas
- Kloroplas
PERUBAHAN PLASTIDA PADA BUAH

From U. Wisconsin Botany Dept.


KLOROPLAS
KLOROPLAS

Berada pada sel tumbuhan, protozoa, bakteri,


jamur
Letak kloroplas pd tumbuhan mesofil
(daging) daun
mengandung klorofil a & klorofil b, DNA & RNA
Bentuk dan ukuran Kloroplas bervariasi
menurut species
Jumlah Kloroplas bervariasi tergantung tipe
sel dan fisiologis sel
PROSES FOTOSINTESIS
Light
Stroma

Stack of NADP
thylakoids ADP
+P
Light Calvin
reactions cycle

Sugar used for


Cellular respiration
Cellulose
Starch
Other organic compounds
MITOKONDRIA
HUMAN NUCLEAR
MITOCHONDRIAL GENOMES
NUCLEAR GENOME MITOCHONDRIAL
GENOME
Size 3200 Mb 16.6 kb

No. of different 23 (in XX cells) or 24 One circular DNA


DNA molecules (in XY cells); all linear molecule

Total no. of DNA 46 in diploid cells, but Often several


molecules per cell varies according to thousands (but variable
ploidy
Associated protein Several classes of Largely free of protein
histone & nonhistone
protein
No. of genes ~ 30 000 ~35-000 37

Gene density ~ 1/100 kb 1/0.45 kb


Mitochondria are responsible for producing
most of the energy that's needed for our cells
to function
A mitochondrial disease can shut down some
or all the mitochondria, cutting off this
essential energy supply.
Mitochondrial DNA (mtDNA) mutations is
thought to be the reason which cause
mitochondria disease
MITOCHONDRIAL DISEASES

MELAS (Mitochondrial Encephalomyopathy with


Lactic Acidosis and Stroke-like episodes
MERRF (Myoclonic Epilepsy with Ragged Red Fibres)
Leber Hereditary Optic Neuropathy (LHON)
External Ophthalmoplegia
Kearns-Sayre syndrome
Chronic progressive external ophthalmoplegia
NARP (Neurogenic weakness Ataxia with Retinitis
Pigmentosa)
Mitochondrial DNA mutations in human genetic
disease (Wallace Sci. Amer. 277:40)
Maternal genetic
transmission

An affected woman transmits the trait to


all her children. Affected men
(represented by squares do not pass
the trait to any of their offspring
Problems That May Be Associated with Mitochondrial Cytopathies

Organ Systems Possible Problems

developmental delays, mental retardation, dementia, seizures, neuro-


Brain
psychiatric disturbances, atypical cerebral palsy, migraines, strokes
weakness (which may be intermittent), neuropathic pain, absent reflexes,
dysautonomia, gastrointestinal problems (ge reflux, dysmotility, diarrhea,
Nerves irritable bowel syndrome, constipation, pseudo-obstruction), fainting,
absent or excessive sweating resulting in temperature regulation
problems
Muscles weakness, hypotonia, cramping, muscle pain

renal tubular acidosis or wasting resulting in loss of protein, magnesium,


Kidneys
phosphorous, calcium and other electrolytes.

Heart cardiac conduction defects (heart blocks), cardiomyopathy

Liver hypoglycemia (low blood sugar), liver failure

Eyes visual loss and blindness

Ears hearing loss and deafness

Pancreas and Other diabetes and exocrine pancreatic failure (inability to make digestive
Glands enzymes), parathyroid failure (low calcium)

failure to gain weight, short stature, fatigue, respiratory problems including


Systemic
intermittent air hunger, vomitting
Mitochondrial DNA polymorphisms track human
Migrations (Wallace Sci. Amer. 277:40)

All humans descend from a small group of Africans


This group originated in central Africa ~200,000 years ago
The founding group was small (102-104 people)
Descendants of this group replaced all other hominids everywhere in the world